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  • Cells, Cultured  (1,353)
  • Cell & Developmental Biology
  • Engineering
  • SPACE SCIENCES
  • American Association for the Advancement of Science (AAAS)  (1,400)
  • Solomons, MD  (15)
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  • 1
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    Effects of suspended sediments on the development of eggs and larvae of striped bass and white perch (2021)
    University of Maryland Center for Environmental Science, Chesapeake Biological Laboratory | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/4861 | 130 | 2011-09-29 15:47:49 | 4861 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-07-06
    Description: The possible ecological effects of suspended sediments are manifold. Briefly, suspended sediments may cause an increased surface for microorganism growth, fewer temperature fluctuations, chemical adsorption orabsorption, blanketing, mechanical-abrasive actions, and light penetration reduction (Cairns, 1968). Sherk and Cronin (1970) have pointed out that the above effects have been little studied in the estuarine environment. The ecological effects of suspended sediments on fish eggs and larvae may be of prime importance t o the C and D Canal area, an important spawning and primary nursery area for a variety of estuary: e species (Johnson,1972). This section discusses the effects of suspended sediment on the eggs and larvae of striped bass and white perch.
    Description: Army Corps of Engineers, Philadelphia District
    Keywords: Conservation ; Ecology ; Engineering ; Fisheries ; Chesapeake ; Canal ; Natural Resources Institute ; Striped Bass ; White Perch ; Delaware
    Repository Name: AquaDocs
    Type: monograph
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  • 2
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    Enabling Sensor* Interoperability, Portland, Maine, October 16-18 2006: workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3112 | 130 | 2011-09-29 17:51:50 | 3112 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-07-01
    Description: The ACT workshop "Enabling Sensor Interoperability" addressed the need for protocols at thehardware, firmware, and higher levels in order to attain instrument interoperability within and betweenocean observing systems. For the purpose of the workshop, participants spoke in tern of "instruments" rather than "sensors," defining an instrument as a device that contains one or more sensors or actuators and can convert signals from analog to digital.An increase in the abundance, variety, and complexity of instruments and observing systems suggeststhat effective standards would greatly improve "plug-and-work" capabilities. However, there are few standards or standards bodies that currently address instrument interoperability and configuration.Instrument interoperability issues span the length and breadth of these systems, from the measurementto the end user, including middleware services. There are three major components of instrumentinteroperability including physical, communication, and application/control layers. Participantsidentified the essential issues, current obstacles, and enabling technologies and standards,then came up with a series of short and long term solutions.The top three recommended actions, deemed achievable within 6 months of the release of thisreport are:A list of recommendations for enabling instrument interoperability should be put togetherand distributed to instrument developers.A recommendation for funding sources to achieve instrument interoperability should bedrafted. Funding should be provided (for example through NOPP or an IOOS request forproposals) to develop and demonstrate instrument interoperability technologies involvinginstrument manufacturers, observing system operators, and cyberinfrastructure groups.Program managers should be identified and made to understand that milestones for achievinginstrument interoperability include a) selection of a methodology for uniquely identifyingan instrument, b) development of a common protocol for automatic instrumentdiscovery, c) agreement on uniform methods for measurements, d) enablement of end usercontrolled power cycling, and e) implementation of a registry component for IDS and attributes.The top three recommended actions, deemed achievable within S years of the release of this reportare:An ocean observing interoperability standards body should be established that addresses standards for a) metadata, b) commands, c) protocols, d) processes, e) exclusivity, and f)naming authorities.[PDF contains 48 pages]
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Engineering ; Environment
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  • 3
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    Meteorological Buoy Sensor Workshop, Solomons, Maryland, April 19-21, 2006: workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3115 | 130 | 2011-09-29 17:52:01 | 3115
    Details
    Publication Date: 2021-07-01
    Description: The co-organized Alliance for Coastal Technologies (ACT) and National Data Buoy Center (NDBC)Workshop "Meteorological Buoy Sensors Workshop" convened in Solomons, Maryland, April 19to 21,2006, sponsored by the University of Maryland Center for Environmental Science (UMCES)Chesapeake Bay Laboratory (CBL), an ACT partner institution. Participants from various sectorsincluding resource managers and industry representatives collaborated to focus on technologies andsensors that measure the near surface variables of wind speed and direction, barometric pressure,humidity and air temperature. The vendor list was accordingly targeted at companies that producedthese types of sensors. The managers represented a cross section of federal, regional and academicmarine observing interests from around the country. Workshop discussions focused on the challengesassociated with making marine meteorological observations in general and problems that werespecific to a particular variable. Discussions also explored methods to mitigate these challengesthrough the adoption of best practices, improved technologies and increased standardization. Someof the key workshop outcomes and recommendations included:0cean.US should establish a committee devoted to observations. The committee wouldhave a key role in developing observing standards.The community should adopt the target cost, reliability and performance standards draftedfor a typical meteorological package to be used by a regional observing system.A forum should be established to allow users and manufacturers to share best practicesfor the employment of marine meteorological sensors. The ACT website would host theforum.Federal activities that evaluate meteorological sensors should make their results publiclyavailable.ACT should extend their evaluation process to include meteorological sensors.A follow on workshop should be conducted that covers the observing of meteorologicalvariables not addressed by this workshop. (pdf contains 18 pages)
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Engineering ; Environment
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  • 4
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    Evaluating approaches and technologies for monitoring organic contaminants in the aquatic environment, Ann Arbor, MI, July 21-23, 2006: workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3114 | 130 | 2011-09-29 17:51:58 | 3114 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-07-01
    Description: The Alliance for Coastal Technologies (ACT) convened a workshop on Evaluating Approaches and Technologies for Monitoring Organic Contaminants in the Aquatic Environment in Ann Arbor, MI on July 21-23, 2006. The primary objectives of this workshop were to: 1) identify the priority management information needs relative to organic contaminant loading; 2) explore themost appropriate approaches to estimating mass loading; and 3) evaluate the current status of thesensor technology. To meet these objectives, a mixture of leading research scientists, resourcemanagers, and industry representatives were brought together for a focused two-day workshop.The workshop featured four plenary talks followed by breakout sessions in which arranged groupsof participants where charged to respond to a series of focused discussion questions.At present, there are major concerns about the inadequacies in approaches and technologies forquantifying mass emissions and detection of organic contaminants for protecting municipal watersupplies and receiving waters. Managers use estimates of land-based contaminant loadings torivers, lakes, and oceans to assess relative risk among various contaminant sources, determinecompliance with regulatory standards, and define progress in source reduction. However, accuratelyquantifying contaminant loading remains a major challenge. Loading occurs over a range ofhydrologic conditions, requiring measurement technologies that can accommodate a broad rangeof ambient conditions. In addition, in situ chemical sensors that provide a means for acquiringcontinuous concentration measurements are still under development, particularly for organic contaminantsthat typically occur at low concentrations. Better approaches and strategies for estimatingcontaminant loading, including evaluations of both sampling design and sensor technologies,need to be identified. The following general recommendations were made in an effort to advancefuture organic contaminant monitoring:1. Improve the understanding of material balance in aquatic systems and the relationship betweenpotential surrogate measures (e.g., DOC, chlorophyll, particle size distribution) and target constituents.2. Develop continuous real-time sensors to be used by managers as screening measures and triggersfor more intensive monitoring.3. Pursue surrogate measures and indicators of organic pollutant contamination, such as CDOM,turbidity, or non-equilibrium partitioning.4. Develop continuous field-deployable sensors for PCBs, PAHs, pyrethroids, and emerging contaminantsof concern and develop strategies that couple sampling approaches with tools that incorporatesensor synergy (i.e., measure appropriate surrogates along with the dissolved organics toallow full mass emission estimation).[PDF contains 20 pages]
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Engineering ; Earth Sciences ; Environment ; Chemistry
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  • 5
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    Transfer of Medical Sensor Technologies to Environmental Monitoring, Solomons, Maryland, April 6-8, 2005: workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3123 | 130 | 2011-09-29 17:52:46 | 3123 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-06-25
    Description: (pdf contains 23 pages)
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Engineering ; Environment
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  • 6
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    Dissolved oxygen probes: making oxygen measurements routine like temperature, St Petersburg, Florida, January 4-6, 2006: workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3118 | 130 | 2011-09-29 17:52:37 | 3118 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-06-25
    Description: The Alliance for Coastal Technologies (ACT) Workshop "Making Oxygen MeasurementsRoutine Like Temperature" was convened in St. Petersburg, Florida, January 4th - 6th, 2006. Thisevent was sponsored by the University of South Florida (USF) College of Marine Science, anACT partner institution and co-hosted by the Ocean Research Interactive Observatory Networks(ORION). Participants from researcldacademia, resource management, industry, and engineeringsectors collaborated with the aim to foster ideas and information on how to make measuringdissolved oxygen a routine part of a coastal or open ocean observing system.Plans are in motion to develop large scale ocean observing systems as part of the US IntegratedOcean Observing System (100s; see http://ocean.us) and the NSF Ocean Observatory Initiative(001; see http://www.orionprogram.org/00I/default.hl). These systems will require biologicaland chemical sensors that can be deployed in large numbers, with high reliability, and forextended periods of time (years). It is also likely that the development cycle for new sensors issufficiently long enough that completely new instruments, which operate on novel principles,cannot be developed before these complex observing systems will be deployed. The most likelypath to development of robust, reliable, high endurance sensors in the near future is to movethe current generation of sensors to a much greater degree of readiness. The ACT OxygenSensor Technology Evaluation demonstrated two important facts that are related to the need forsensors. There is a suite of commercially available sensors that can, in some circumstances,generate high quality data; however, the evaluation also showed that none of the sensors were ableto generate high quality data in all circumstances for even one month time periods due tobiofouling issues.Many groups are attempting to use oxygen sensors in large observing programs; however, thereoften seems to be limited communication between these groups and they often do not have accessto sophisticated engineering resources. Instrument manufacturers also do not have sufficientresources to bring sensors, which are marketable, but of limited endurance or reliability, to ahigher state of readiness. The goal of this ACT/ORION Oxygen Sensor Workshop was to bringtogether a group of experienced oceanographers who are now deploying oxygen sensors inextended arrays along with a core of experienced and interested academic and industrialengineers, and manufacturers. The intended direction for this workshop was for this group toexchange information accumulated through a variety of sensor deployments, examine failuremechanisms and explore a variety of potential solutions to these problems. One anticipatedoutcome was for there to be focused recommendations to funding agencies on development needsand potential solutions for 02 sensors. (pdf contains 19 pages)
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Engineering ; Environment
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  • 7
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    Towed vehicles: undulating platforms as tools for maping coastal processes and water quality assessment, Seaside, California, February 5-7,2007. Workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3106 | 130 | 2011-09-29 17:51:19 | 3106 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-07-01
    Description: The Alliance for Coastal Technologies (ACT) Workshop on Towed Vehicles: Undulating PlatformsAs Tools for Mapping Coastal Processes and Water Quality Assessment was convenedFebruary 5-7,2007 at The Embassy Suites Hotel, Seaside, California and sponsored by the ACT-PacificCoast partnership at the Moss Landing Marine Laboratories (MLML). The TUV workshopwas co-chaired by Richard Burt (Chelsea Technology Group) and Stewart Lamerdin (MLMLMarine Operations). Invited participants were selected to provide a uniform representation of theacademic researchers, private sector product developers, and existing and potential data productusers from the resource management community to enable development of broad consensus opinionson the application of TUV platforms in coastal resource assessment and management.The workshop was organized to address recognized limitations of point-based monitoring programs,which, while providing valuable data, are incapable of describing the spatial heterogeneityand the extent of features distributed in the bulk solution. This is particularly true as surveysapproach the coastal zone where tidal and estuarine influences result in spatially and temporallyheterogeneous water masses and entrained biological components. Aerial or satellite based remotesensing can provide an assessment of the aerial extent of plumes and blooms, yet provide no informationregarding the third dimension of these features. Towed vehicles offer a cost-effectivesolution to this problem by providing platforms, which can sample in the horizontal, vertical, andtime-based domains. Towed undulating vehicles (henceforth TUVs) represent useful platformsfor event-response characterization. This workshop reviewed the current status of towed vehicletechnology focusing on limitations of depth, data telemetry, instrument power demands, and shiprequirements in an attempt to identify means to incorporate such technology more routinely inmonitoring and event-response programs. Specifically, the participants were charged to addressthe following: (1) Summarize the state of the art in TUV technologies; (2) Identify how TUVplatforms are used and how they can assist coastal managers in fulfilling their regulatory and managementresponsibilities; (3) Identify barriers and challenges to the application of TUV technologiesin management and research activities, and (4) Recommend a series of community actions toovercome identified barriers and challenges.A series of plenary presentation were provided to enhance subsequent breakout discussions bythe participants. Dave Nelson (University of Rhode Island) provided extensive summaries andreal-world assessment of the operational features of a variety of TUV platforms available in theUNOLs scientific fleet. Dr. Burke Hales (Oregon State University) described the modification ofTUV to provide a novel sampling platform for high resolution mapping of chemical distributionsin near real time. Dr. Sonia Batten (Sir Alister Hardy Foundation for Ocean Sciences) providedan overview on the deployment of specialized towed vehicles equipped with rugged continuousplankton recorders on ships of opportunity to obtain long-term, basin wide surveys of zooplanktoncommunity structure, enhancing our understanding of trends in secondary production in the upperocean. [PDF contains 32 pages]
    Description: NOAA
    Keywords: Engineering ; Environment ; Planning
    Repository Name: AquaDocs
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  • 8
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    Recent Developments in In Situ Nutrient Sensors: applications and future directions, Savannah, Georgia, December 11-13, 2006: workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3111 | 130 | 2011-09-29 17:51:47 | 3111 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-07-01
    Description: The Alliance for Coastal Technologies (ACT) convened a Workshop on "Recent Developments in In Situ Nutrient Sensors: Applications and Future Directions" from 11-13 December, 2006. The workshop was held at the Georgia Coastal Center in Savannah, Georgia, with local coordination provided by the ACT partner at the Skidaway Institute of Oceanography (University System of Georgia). Since its formation in 2000, ACT partners have been conducting workshops on various sensor technologies and supporting infrastructure for sensor systems. This was the first workshop to revisit a topic area addressed previously by ACT.An earlier workshop on the "State of Technology in the Development and Application of Nutrient Sensors" was held in Savannah, Georgia from 10-12 March, 2003. Participants in the first workshop included representatives from management, industry, and research sectors. Among the topics addressed at the first workshop were characteristics of "ideal" in situ nutrient sensors, particularly with regard to applications in coastal marine waters.In contrast, the present workshop focused on the existing commercial solutions. The in situ nutrient sensor technologies that appear likely to remain the dominant commercial options for the next decade are reagent-based in situ auto-analyzers (or fluidics systems) and an optical approach (spectrophotometric measurement of nitrate). The number of available commercial systems has expanded since 2003, and community support for expanded application and further development of these technologies appears warranted. Application in coastal observing systems, including freshwater as well as estuarine and marine environments, was a focus of the present workshop.This included discussion of possible refinements for sustained deployments as part of integrated instrument packages and means to better promote broader use of nutrient sensors in observing system and management applications. The present workshop also made a number of specific recommendations concerning plans for a demonstration of in situ nutrient sensor technologies that ACT will be conducting in coordination with sensor manufacturers.[PDF contains 40 pages]
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Engineering ; Environment
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  • 9
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    Measures of turbidity in coastal waters, Coconut Island, Oahu, Hawaii, August 31 - September 2, 2005: workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3120 | 130 | 2011-09-29 17:52:40 | 3120 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-06-25
    Description: A three day workshop on turbidity measurements was held at the Hawaii Institute of MarineBiology from August 3 1 to September 2, 2005. The workshop was attended by 30 participantsfrom industry, coastal management agencies, and academic institutions. All groups recognizedcommon issues regarding the definition of turbidity, limitations of consistent calibration, and thelarge variety of instrumentation that nominally measure "turbidity." The major recommendations,in order of importance for the coastal monitoring community are listed below:1. The community of users in coastal ecosystems should tighten instrument designconfigurations to minimize inter-instrument variability, choosing a set of specificationsthat are best suited for coastal waters. The IS0 7027 design standard is not tight enough.Advice on these design criteria should be solicited through the ASTM as well as Federaland State regulatory agencies representing the majority of turbidity sensor end users.Parties interested in making turbidity measurements in coastal waters should developdesign specifications for these water types rather than relying on design standards madefor the analysis of drinking water.2. The coastal observing groups should assemble a community database relating output ofspecific sensors to different environmental parameters, so that the entire community ofusers can benefit from shared information. This would include an unbiased, parallel studyof different turbidity sensors, employing a variety of designs and configuration in thebroadest range of coastal environments.3. Turbidity should be used as a measure of relative change in water quality rather than anabsolute measure of water quality. Thus, this is a recommendation for managers todevelop their own local calibrations. See next recommendation.4. If the end user specifically wants to use a turbidity sensor to measure a specific waterquality parameter such as suspended particle concentration, then direct measurement ofthat water quality parameter is necessary to correlate with 'turbidity1 for a particularenvironment. These correlations, however, will be specific to the environment in whichthey are measured. This works because there are many environments in which watercomposition is relatively stable but varies in magnitude or concentration. (pdf contains 22 pages)
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Oceanography ; Engineering ; Environment
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  • 10
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    Technologies for Measuring Currents in Coastal Environments, Portland, Maine, October 26-28, 2005:workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3119 | 130 | 2011-09-29 17:52:39 | 3119 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-06-25
    Description: The Alliance for Coastal Technologies (ACT) Workshop entitled "Technologies for MeasuringCurrents in Coastal Environments" was held in Portland, Maine, October 26-28, 2005, withsponsorship by the Gulf of Maine Ocean Observing System (GoMOOS), an ACT partnerorganization. The primary goals of the event were to summarize recent trends in nearshoreresearch and management applications for current meter technologies, identify how currentmeters can assist coastal managers to fulfill their regulatory and management objectives, and torecommend actions to overcome barriers to use of the technologies. The workshop was attendedby 25 participants representing state and federal environmental management agencies,manufacturers of current meter technologies, and researchers from academic institutions andprivate industry.Common themes that were discussed during the workshop included 1) advantages and limitationsof existing current measuring equipment, 2) reliability and ease of use with each instrument type,3) data decoding and interpretation procedures, and 4) mechanisms to facilitate better training andguidance to a broad user group. Seven key recommendations, which were ranked in order ofimportance during the last day of the workshop are listed below.1. Forums should be developed to facilitate the exchange of information among users andindustry:a) On-line forums that not only provide information on specific instruments andtechnologies, but also provide an avenue for the exchange of user experiences withvarious instruments (i.e. problems encountered, cautions, tips, advantages, etc). (seeReferences for manufacturer websites with links to application and technical forums atend of report)b) Regional training/meetings for operational managers to exchange ideas on methods formeasuring currents and evaluating data.c) Organize mini-meetings or tutorial sessions within larger conference venues.2. A committee of major stakeholders should be convened to develop common standards(similar to the Institute of Electrical and Electronics Engineers (IEEE) committee) thatenable users to switch sensors without losing software or display capabilities. (pdf contains 28 pages)
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Oceanography ; Engineering ; Environment
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  • 11
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    Ground water-surface water interactions sensor technology, Savannah, Georgia, March 7-9, 2005: workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3124 | 130 | 2011-09-29 17:52:48 | 3124 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-06-25
    Description: The Alliance for Coastal Technologies (ACT) held a Workshop on Sensor Technology forAssessing Groundwater-Surface Water Interactions in the Coastal Zone on March 7 to 9,2005 inSavannah, GA. The main goal of the workshop was to summarize the general parameters, whichhave been found to be useful in assessing groundwater-surface water (GW-SW) interactions in thecoastal zone. The workshop participants (Appendix I) were specifically charged with identifyingthe types of sensor systems, if any, that have been used to obtain time-series data and to makeknown which parameters may be the most amenable to the development/application of sensortechnology. The group consisted of researchers, industry representatives, and environmentalmanagers.Four general recommendations were made:1. Educate coastal managers and agencies on the importance of GW-SW interactions,keeping in mind that regulatory agencies are driven by a different set of rules thanresearchers: the focus is on understanding the significance of the problem and providingsolutions. ACT could facilitate this process in two ways. First, given that the researchliterature on this subject is fairly diffuse, ACT could provide links from its web site to factsheets or other literature. Second, ACT could organize a focused meeting for managersand/or agency groups.Encourage development of primary tools for quantifying flow. The most promisingtechnology in this respect is flow meters designed for flux chambers, mainly because theyshould be simple to use and can be made relatively inexpensively. However, it should bekept in mind that they provide only point measurements and several would need to bedeployed as a network in order to obtain reliable flow estimates. For evaluating systemwide GW-SW interactions, tools that integrate the signal over large areas would berequired. Suggestions include a user-friendly hydrogeologic models, keeping in mind thatfreshwater flow is not the entire story, or continuous radon monitors. Though the latterwould be slightly more difficult to use in terms of background knowledge, such aninstrument would be low power and easy to operate and maintain. ACT could facilitatethis recommendation by identifying funding opportunities on its web site and/orperforming evaluations of existing technologies that could be summarized on the web site. (pdf contains 18 pages)
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Engineering ; Environment
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  • 12
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    Biological Platforms for Environmental Sensor technologies and their uses as indicators of the marine environment, Seward, Alaska, September 19-21, 2007: workshop proceedings (2021)
    Alliance for Coastal Technologies(ACT) | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3109 | 130 | 2011-09-29 17:51:40 | 3109 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-07-01
    Description: The Alliance for Coastal Technologies (ACT) Workshop entitled, "Biological Platforms as Sensor Technologies and their Use as Indicators for the Marine Environment" was held in Seward, Alaska, September 19 - 21,2007. The workshop was co-hosted by the University of Alaska Fairbanks (UAF) and the Alaska SeaLife Center (ASLC). The workshop was attended by 25 participants representing a wide range of research scientists, managers, and manufacturers who develop and deploy sensory equipment using aquatic vertebrates as the mode of transport.Eight recommendations were made by participants at the conclusion of the workshop and are presentedhere without prioritization:1. Encourage research toward development of energy scavenging devices of suitable sizes foruse in remote sensing packages attached to marine animals.2. Encourage funding sources for development of new sensor technologies and animal-bornetags.3. Develop animal-borne environmental sensor platforms that offer more combined systemsand improved data recovery methodologies, and expand the geographic scope of complementaryfixed sensor arrays.4. Engage the oceanographic community by:a. Offering a mini workshop at an AGU ocean sciences conference for people interestedin developing an ocean carbon program that utilizes animal-borne sensor technology.b. Outreach to chemical oceanographers.5. Min v2d6.sheepserver.net e and merge technologies from other disciplines that may be appliedto marine sensors (e.g. biomedical field).6. Encourage the NOAA Permitting Office to:a. Make a more predictable, reliable, and consistent permitting system for using animalplatforms.b. Establish an evaluation process.c. Adhere to established standards.7. Promote the expanded use of calibrated hydrophones as part of existing animal platforms.8. Encourage the Integrated Ocean Observing System (IOOS) to promote animal tracking aseffective samplers of the marine environment, and use of animals as ocean sensor technologyplatforms. [PDF contains 20 pages]
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Oceanography ; Engineering ; Environment
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  • 13
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    Optical Remote Sensing of Coastal Habitats, Moss Landing, California, 9-11 January, 2006: workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3117 | 130 | 2011-09-29 17:52:04 | 3117 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-06-25
    Description: The Alliance for Coastal Technologies (ACT) Workshop on Optical Remote Sensing of CoastalHabitats was convened January 9-11, 2006 at Moss Landing Marine Laboratories in MossLanding, California, sponsored by the ACT West Coast regional partnership comprised of theMoss Landing Marine Laboratories (MLML) and the Monterey Bay Aquarium Research Institute(MBARI). The "Optical Remote Sensing of Coastal Habitats" (ORS) Workshop completesACT'S Remote Sensing Technology series by building upon the success of ACT'S West CoastRegional Partner Workshop "Acoustic Remote Sensing Technologies for Coastal Imaging andResource Assessment" (ACT 04-07). Drs. Paul Bissett of the Florida Environmental ResearchInstitute (FERI) and Scott McClean of Satlantic, Inc. were the ORS workshop co-chairs. Invitedparticipants were selected to provide a uniform representation of the academic researchers, privatesector product developers, and existing and potential data product users from the resource managementcommunity to enable development of broad consensus opinions on the role of ORS technologiesin coastal resource assessment and management.The workshop was organized to examine the current state of multi- and hyper-spectral imagingtechnologies with the intent to assess the current limits on their routine application for habitat classificationand resource monitoring of coastal watersheds, nearshore shallow water environments,and adjacent optically deep waters. Breakout discussions focused on the capabilities, advantages,and limitations of the different technologies (e.g., spectral & spatial resolution), as well as practicalissues related to instrument and platform availability, reliability, hardware, software, and technicalskill levels required to exploit the data products generated by these instruments. Specifically,the participants were charged to address the following: (1) Identify the types of ORS data productscurrently used for coastal resource assessment and how they can assist coastal managers in fulfillingtheir regulatory and management responsibilities; (2) Identify barriers and challenges to theapplication of ORS technologies in management and research activities; (3) Recommend a seriesof community actions to overcome identified barriers and challenges.Plenary presentations by Drs. Curtiss 0. Davis (Oregon State University) and Stephan Lataille(ITRES Research, Ltd.) provided background summaries on the varieties of ORS technologiesavailable, deployment platform options, and tradeoffs for application of ORS data products withspecific applications to the assessment of coastal zone water quality and habitat characterization.Dr. Jim Aiken (CASIX) described how multiscale ground-truth measurements were essential fordeveloping robust assessment of modeled biogeochemical interpretations derived from opticallybased earth observation data sets. While continuing improvements in sensor spectral resolution,signal to noise and dynamic range coupled with sensor-integrated GPS, improved processing algorithmsfor georectification, and atmospheric correction have made ORS data products invaluablesynoptic tools for oceanographic research, their adoption as management tools has lagged. SethBlitch (Apalachicola National Estuarine Research Reserve) described the obvious needs for, yetsubstantial challenges hindering the adoption of advanced spectroscopic imaging data productsto supplement the current dominance of digital ortho-quad imagery by the resource managementcommunity, especially when they impinge on regulatory issues. (pdf contains 32 pages)
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Engineering ; Environment
    Repository Name: AquaDocs
    Type: monograph
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    Trace Metal Sensors for Coastal Monitoring, Seaside, California, April 11-13, 2005: workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3122 | 130 | 2011-09-29 17:52:44 | 3122 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-06-25
    Description: The Alliance for Coastal Technologies (ACT) Workshop on Trace Metal Sensors for CoastalMonitoring was convened April 11-13, 2005 at the Embassy Suites in Seaside, California withpartnership from Moss Landing Marine Laboratories (MLML) and the Monterey Bay AquariumResearch Institute (MBARI).Trace metals play many important roles in marine ecosystems. Due to their extreme toxicity, theeffects of copper, cadmium and certain organo-metallinc compounds (such as tributyltin andmethylmercury) have received much attention. Lately, the sublethal effects of metals onphytoplankton biochemistry, and in some cases the expression of neurotoxins (Domoic acid),have been shown to be important environmental forcing functions determining the compositionand gene expression in some groups. More recently the role of iron in controlling phytoplanktongrowth has led to an understanding of trace metal limitation in coastal systems. Although metalsplay an important role at many different levels, few technologies exist to provide rapid assessmentof metal concentrations or metal speciation in the coastal zone where metal-induced toxicity orpotential stimulation of harmful algal blooms, can have major economic impacts. This workshopfocused on the state of on-site and in situ trace element detection technologies, in terms of whatis currently working well and what is needed to effectively inform coastal zone managers, as wellas guide adaptive scientific sampling of the coastal zone. Specifically the goals of this workshopwere to: 1) summarize current regional requirements and future targets for metal monitoring infreshwater, estuarine and coastal environments; 2) evaluate the current status of metal sensors andpossibilities for leveraging emerging technologies for expanding detection limits and targetelements; and 3) help identify critical steps needed for and limits to operational deployment ofmetal sensors as part of routine water quality monitoring efforts.Following a series of breakout group discussions and overview talks on metal monitoringregulatory issues, analytical techniques and market requirements, workshop participants madeseveral recommendations for steps needed to foster development of in situ metal monitoringcapacities:1. Increase scientific and public awareness of metals of environmental and biologicalconcern and their impacts in aquatic environments. Inform scientific and publiccommunities regarding actual levels of trace metals in natural and perturbed systems.2. Identify multiple use applications (e.g., industrial waste steam and drinking water qualitymonitoring) to support investments in metal sensor development. (pdf contains 27 pages)
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Engineering ; Environment
    Repository Name: AquaDocs
    Type: monograph
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    Seabed Sensor Technology, Savannah, Georgia, February 1-3, 2006: workshop proceedings (2021)
    Alliance for Coastal Technologies | Solomons, MD
    In:  http://aquaticcommons.org/id/eprint/3239 | 130 | 2011-09-29 17:41:57 | 3239 | University of Maryland Center for Environmental Science. Chesapeake Biological Laboratory
    Details
    Publication Date: 2021-06-26
    Description: Future coastal management practices require that a holistic, ecosystem management approach beadopted. Coastal ecosystems, however, present a variety of specific and unique challengesrelative to open ocean systems. In particular, interactions with the seabed significantly influencethe coastal ecosystem. Observing technologies must be developed and employed to incorporateseafloor interactions, processes and habitat diversity into research and management activities.An ACT Workshop on Seabed Sensor Technology was held February 1-3, 2006 in Savannah,Georgia, to summarize the current state of sensor technologies applicable to examining andmonitoring the coastal seabed, including the near-bed benthic boundary layer and surfacesediment layer. Workshop participants were specifically charged to identify current sensors inuse, recommend improvements to these systems and to identify areas for future development andactivities that would advance the use of sensor technology in the observation, monitoring andmanagement of the coastal benthic environment. (pdf contains 23 pages)
    Description: NOAA
    Description: Alliance for Coastal Technologies, CBL/UMCES
    Keywords: Oceanography ; Engineering ; Environment
    Repository Name: AquaDocs
    Type: monograph
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    Spraying makes it smoother (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-17
    Keywords: Engineering
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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    3D printed polyamide membranes for desalination (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-08-17
    Description: Polyamide thickness and roughness have been identified as critical properties that affect thin-film composite membrane performance for reverse osmosis. Conventional formation methodologies lack the ability to control these properties independently with high resolution or precision. An additive approach is presented that uses electrospraying to deposit monomers directly onto a substrate, where they react to form polyamide. The small droplet size coupled with low monomer concentrations result in polyamide films that are smoother and thinner than conventional polyamides, while the additive nature of the approach allows for control of thickness and roughness. Polyamide films are formed with a thickness that is controllable down to 4-nanometer increments and a roughness as low as 2 nanometers while still exhibiting good permselectivity relative to a commercial benchmarking membrane.
    Keywords: Engineering
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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    Zeolitic imidazolate framework membranes made by ligand-induced permselectivation (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-09-07
    Description: Zeolitic imidazolate framework (ZIF) membranes are emerging as a promising energy-efficient separation technology. However, their reliable and scalable manufacturing remains a challenge. We demonstrate the fabrication of ZIF nanocomposite membranes by means of an all-vapor-phase processing method based on atomic layer deposition (ALD) of ZnO in a porous support followed by ligand-vapor treatment. After ALD, the obtained nanocomposite exhibits low flux and is not selective, whereas after ligand-vapor (2-methylimidazole) treatment, it is partially transformed to ZIF and shows stable performance with high mixture separation factor for propylene over propane (an energy-intensive high-volume separation) and high propylene flux. Membrane synthesis through ligand-induced permselectivation of a nonselective and impermeable deposit is shown to be simple and highly reproducible and holds promise for scalability.
    Keywords: Engineering
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    Robotic-flapper maneuvers and fruitfly turns (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-09-14
    Keywords: Engineering
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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    A tailless aerial robotic flapper reveals that flies use torque coupling in rapid banked turns (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-09-14
    Description: Insects are among the most agile natural flyers. Hypotheses on their flight control cannot always be validated by experiments with animals or tethered robots. To this end, we developed a programmable and agile autonomous free-flying robot controlled through bio-inspired motion changes of its flapping wings. Despite being 55 times the size of a fruit fly, the robot can accurately mimic the rapid escape maneuvers of flies, including a correcting yaw rotation toward the escape heading. Because the robot’s yaw control was turned off, we showed that these yaw rotations result from passive, translation-induced aerodynamic coupling between the yaw torque and the roll and pitch torques produced throughout the maneuver. The robot enables new methods for studying animal flight, and its flight characteristics allow for real-world flight missions.
    Keywords: Engineering
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    Hop, skip, jump, or massive leap (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-04-27
    Keywords: Engineering
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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    Flying fast and free (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-09-14
    Keywords: Engineering
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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    Behind the scenes of the built environment (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2018-03-09
    Keywords: Engineering
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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    The art of manufacturing molecules (2018)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2018-01-19
    Keywords: Engineering
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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    Fast exoskeleton optimization (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-06-23
    Keywords: Engineering
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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    Optimum human input (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-06-23
    Keywords: Engineering
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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    Filtering through to what's important (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-06-16
    Keywords: Engineering
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 28
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    Human-in-the-loop optimization of exoskeleton assistance during walking (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-06-23
    Description: Exoskeletons and active prostheses promise to enhance human mobility, but few have succeeded. Optimizing device characteristics on the basis of measured human performance could lead to improved designs. We have developed a method for identifying the exoskeleton assistance that minimizes human energy cost during walking. Optimized torque patterns from an exoskeleton worn on one ankle reduced metabolic energy consumption by 24.2 ± 7.4% compared to no torque. The approach was effective with exoskeletons worn on one or both ankles, during a variety of walking conditions, during running, and when optimizing muscle activity. Finding a good generic assistance pattern, customizing it to individual needs, and helping users learn to take advantage of the device all contributed to improved economy. Optimization methods with these features can substantially improve performance.
    Keywords: Engineering
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    Making the future (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-11-24
    Keywords: Engineering
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  • 30
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    Comment on "Water harvesting from air with metal-organic frameworks powered by natural sunlight" (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-12-01
    Description: Kim et al . (Reports, 28 April 2017, p. 430) presented results for the solar-driven harvesting of water from air via metal-organic frameworks as a prodigious potential advance toward remedying global water shortages. Basic thermodynamics and a survey of multiple off-the-shelf technologies show that their approach is vastly inferior in efficiency (and thereby in feasibility) to available alternatives.
    Keywords: Engineering
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    To frack or not to frack (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-12-01
    Keywords: Engineering
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 32
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    Response to Comment on "Water harvesting from air with metal-organic frameworks powered by natural sunlight" (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-12-01
    Description: In their comment, Bui et al . argue that the approach we described in our report is vastly inferior in efficiency to alternative off-the-shelf technologies. Their conclusion is invalid, as they compare efficiencies in completely different operating conditions. Here, using heat transfer and thermodynamics principles, we show how Bui et al .’s conclusions about the efficiencies of off-the-shelf technologies are fundamentally flawed and inaccurate for the operating conditions described in our study.
    Keywords: Engineering
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    Coupling between distant biofilms and emergence of nutrient time-sharing (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2017-05-12
    Description: Bacteria within communities can interact to organize their behavior. It has been unclear whether such interactions can extend beyond a single community to coordinate the behavior of distant populations. We discovered that two Bacillus subtilis biofilm communities undergoing metabolic oscillations can become coupled through electrical signaling and synchronize their growth dynamics. Coupling increases competition by also synchronizing demand for limited nutrients. As predicted by mathematical modeling, we confirm that biofilms resolve this conflict by switching from in-phase to antiphase oscillations. This results in time-sharing behavior, where each community takes turns consuming nutrients. Time-sharing enables biofilms to counterintuitively increase growth under reduced nutrient supply. Distant biofilms can thus coordinate their behavior to resolve nutrient competition through time-sharing, a strategy used in engineered systems to allocate limited resources.
    Keywords: Engineering
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    Maximizing growth by sharing (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2017-05-12
    Keywords: Engineering
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    [Book Review] Building the future (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2017-02-17
    Description: Engineering has an image problem. The phrase "engineering disaster" rolls off the tongue, while great technical achievements are more often heralded as "scientific miracles." Enter Dream Big. Sponsored by the American Society of Civil Engineers with support from Bechtel Corporation, the film sets out to reframe engineering as a force for good and a profession in service to people and the planet. Author: Donna Riley
    Keywords: Engineering
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    A cirrus cloud climate dial? (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2017-07-21
    Keywords: Engineering
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    Sulfur injections for a cooler planet (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2017-07-21
    Keywords: Engineering
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    Turbines can use CO2 to cut CO2 (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2017-05-26
    Keywords: Engineering
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    Engineered emotions (2017)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2017-11-10
    Keywords: Engineering
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  • 40
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    [Perspective] Solar-powering the Internet of Things (2016)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2016-07-08
    Description: The Internet connects billions of computational platforms of various sizes, from supercomputers to smart phones. However, the same types of data transmission can connect computational resources to much simpler sensors “at the edge of the net” that collect, analyze, and transmit data, as well as controllers that receive instructions. Devices deployed in the environment, homes and offices, and even our bodies would expand the number of connected devices to the trillions. This “Internet of Things” (IoT) underlies the vision of smart homes and buildings that could sense and transmit their status and respond appropriately (1), or track and report on the state of objects (vehicles, goods, or even animals) in the environment. However, the practical implementation of the IoT has been relatively slow, in part because all of these edge devices must draw electrical power from their local environment. We analyze the use of photovoltaics (PV) to power devices and help bring the IoT to fruition. Authors: Richard Haight, Wilfried Haensch, Daniel Friedman
    Keywords: Engineering
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    [Book Review] A monumental challenge (2016)
    American Association for the Advancement of Science (AAAS)
    In: Science
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    Publication Date: 2016-04-22
    Description: So prized by the ancient Romans were Egyptian obelisks that, at one time, more of them stood in Rome than in Egypt. In the 19th century, France, Britain, and the United States—inspired by Napoleon Bonaparte's expedition to Egypt in 1798— acquired their own major obelisks from Alexandria and Luxor. Cleopatra's Needles, by Egyptologist Bob Brier, explores the engineering challenges associated with building and erecting these massive monuments. Author: Andrew Robinson
    Keywords: Engineering
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    Sequential ionic and conformational signaling by calcium channels drives neuronal gene expression (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-02-26
    Description: Voltage-gated CaV1.2 channels (L-type calcium channel alpha1C subunits) are critical mediators of transcription-dependent neural plasticity. Whether these channels signal via the influx of calcium ion (Ca(2+)), voltage-dependent conformational change (VDeltaC), or a combination of the two has thus far been equivocal. We fused CaV1.2 to a ligand-gated Ca(2+)-permeable channel, enabling independent control of localized Ca(2+) and VDeltaC signals. This revealed an unexpected dual requirement: Ca(2+) must first mobilize actin-bound Ca(2+)/calmodulin-dependent protein kinase II, freeing it for subsequent VDeltaC-mediated accumulation. Neither signal alone sufficed to activate transcription. Signal order was crucial: Efficiency peaked when Ca(2+) preceded VDeltaC by 10 to 20 seconds. CaV1.2 VDeltaC synergistically augmented signaling by N-methyl-d-aspartate receptors. Furthermore, VDeltaC mistuning correlated with autistic symptoms in Timothy syndrome. Thus, nonionic VDeltaC signaling is vital to the function of CaV1.2 in synaptic and neuropsychiatric processes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Li, Boxing -- Tadross, Michael R -- Tsien, Richard W -- New York, N.Y. -- Science. 2016 Feb 19;351(6275):863-7. doi: 10.1126/science.aad3647.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. ; Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA. Janelia Research Campus, Howard Hughes Medical Institute, Ashburn, VA 20147, USA. tadrossm@janelia.hhmi.org. ; Department of Neuroscience and Physiology and New York University Neuroscience Institute, New York, NY 10016, USA. Department of Molecular and Cellular Physiology, Beckman Center, School of Medicine, Stanford University, Stanford, CA 94305, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26912895" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Autistic Disorder/genetics/metabolism ; Calcium Channel Blockers/pharmacology ; Calcium Channels, L-Type/chemistry/*metabolism ; *Calcium Signaling ; Calcium-Calmodulin-Dependent Protein Kinase Type 2/*metabolism ; Cells, Cultured ; Cyclic AMP Response Element-Binding Protein/metabolism ; *Gene Expression Regulation ; HEK293 Cells ; Hippocampus/cytology ; Humans ; Long QT Syndrome/genetics/metabolism ; Neuronal Plasticity/*genetics ; Neurons/drug effects/*metabolism ; Nimodipine/pharmacology ; Protein Conformation/drug effects ; Rats ; Rats, Sprague-Dawley ; Receptors, N-Methyl-D-Aspartate/metabolism ; Synapses/metabolism ; Syndactyly/genetics/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Lineage-specific enhancers activate self-renewal genes in macrophages and embryonic stem cells (2016)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2016-01-23
    Description: Differentiated macrophages can self-renew in tissues and expand long term in culture, but the gene regulatory mechanisms that accomplish self-renewal in the differentiated state have remained unknown. Here we show that in mice, the transcription factors MafB and c-Maf repress a macrophage-specific enhancer repertoire associated with a gene network that controls self-renewal. Single-cell analysis revealed that, in vivo, proliferating resident macrophages can access this network by transient down-regulation of Maf transcription factors. The network also controls embryonic stem cell self-renewal but is associated with distinct embryonic stem cell-specific enhancers. This indicates that distinct lineage-specific enhancer platforms regulate a shared network of genes that control self-renewal potential in both stem and mature cells.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Soucie, Erinn L -- Weng, Ziming -- Geirsdottir, Laufey -- Molawi, Kaaweh -- Maurizio, Julien -- Fenouil, Romain -- Mossadegh-Keller, Noushine -- Gimenez, Gregory -- VanHille, Laurent -- Beniazza, Meryam -- Favret, Jeremy -- Berruyer, Carole -- Perrin, Pierre -- Hacohen, Nir -- Andrau, J-C -- Ferrier, Pierre -- Dubreuil, Patrice -- Sidow, Arend -- Sieweke, Michael H -- P01AG036695/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2016 Feb 12;351(6274):aad5510. doi: 10.1126/science.aad5510. Epub 2016 Jan 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Centre de Recherche en Cancerologie de Marseille, INSERM (U1068), CNRS (U7258), Universite Aix-Marseille (UM105), Marseille, France. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu. ; Department of Pathology, Stanford University, Stanford, CA 94305-5324, USA. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Max-Delbruck-Centrum fur Molekulare Medizin in der Helmholtz-Gemeinschaft, 10 Robert-Rossle-Strasse, 13125 Berlin, Germany. ; Broad Institute of Harvard University and MIT, Cambridge, MA 02142, USA. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Institut de Genetique Moleculaire de Montpellier, CNRS UMR 5535, 1919 Route de Mende, 34293 Montpellier, France. ; Centre de Recherche en Cancerologie de Marseille, INSERM (U1068), CNRS (U7258), Universite Aix-Marseille (UM105), Marseille, France. ; Department of Pathology, Stanford University, Stanford, CA 94305-5324, USA. Department of Genetics, Stanford University, Stanford, CA 94305, USA. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu. ; Centre d'Immunologie de Marseille-Luminy, Universite Aix-Marseille, UM2, Campus de Luminy, Case 906, 13288 Marseille Cedex 09, France. INSERM, U1104, Marseille, France. CNRS, UMR 7280, Marseille, France. Max-Delbruck-Centrum fur Molekulare Medizin in der Helmholtz-Gemeinschaft, 10 Robert-Rossle-Strasse, 13125 Berlin, Germany. sieweke@ciml.univ-mrs.fr erinn.soucie@inserm.fr arend@stanford.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26797145" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Differentiation/*genetics ; Cell Lineage/*genetics ; Cell Proliferation ; Cells, Cultured ; Down-Regulation ; Embryonic Stem Cells/*cytology ; Enhancer Elements, Genetic/*physiology ; *Gene Expression Regulation ; Gene Regulatory Networks ; Macrophages/*cytology ; MafB Transcription Factor/metabolism ; Mice ; Proto-Oncogene Proteins c-maf/metabolism ; Single-Cell Analysis ; Transcriptional Activation
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    [Book Review] Street smart (2016)
    American Association for the Advancement of Science (AAAS)
    In: Science
    Details
    Publication Date: 2016-10-21
    Description: A physicist reveals the engineering marvels that underlie the modern metropolis Author: Sybil Derrible
    Keywords: Engineering
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Geosciences , Computer Science , Medicine , Natural Sciences in General , Physics
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    Preventing proteostasis diseases by selective inhibition of a phosphatase regulatory subunit (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-04-11
    Description: Protein phosphorylation regulates virtually all biological processes. Although protein kinases are popular drug targets, targeting protein phosphatases remains a challenge. Here, we describe Sephin1 (selective inhibitor of a holophosphatase), a small molecule that safely and selectively inhibited a regulatory subunit of protein phosphatase 1 in vivo. Sephin1 selectively bound and inhibited the stress-induced PPP1R15A, but not the related and constitutive PPP1R15B, to prolong the benefit of an adaptive phospho-signaling pathway, protecting cells from otherwise lethal protein misfolding stress. In vivo, Sephin1 safely prevented the motor, morphological, and molecular defects of two otherwise unrelated protein-misfolding diseases in mice, Charcot-Marie-Tooth 1B, and amyotrophic lateral sclerosis. Thus, regulatory subunits of phosphatases are drug targets, a property exploited here to safely prevent two protein misfolding diseases.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4490275/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4490275/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Das, Indrajit -- Krzyzosiak, Agnieszka -- Schneider, Kim -- Wrabetz, Lawrence -- D'Antonio, Maurizio -- Barry, Nicholas -- Sigurdardottir, Anna -- Bertolotti, Anne -- 309516/European Research Council/International -- MC_U105185860/Medical Research Council/United Kingdom -- R01-NS55256/NS/NINDS NIH HHS/ -- Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2015 Apr 10;348(6231):239-42. doi: 10.1126/science.aaa4484.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge, CB2 0QH, UK. ; Division of Genetics and Cell Biology, San Raffaele Scientific Institute, 20132 Milan, Italy. ; Medical Research Council Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge, CB2 0QH, UK. aberto@mrc-lmb.cam.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25859045" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/drug therapy/metabolism/pathology ; Animals ; Cells, Cultured ; Charcot-Marie-Tooth Disease/drug therapy/metabolism/pathology ; Disease Models, Animal ; Endoplasmic Reticulum Stress/drug effects ; Enzyme Inhibitors/metabolism/pharmacokinetics/*pharmacology/toxicity ; Guanabenz/*analogs & derivatives/chemical ; synthesis/metabolism/pharmacology/toxicity ; HeLa Cells ; Humans ; Mice ; Mice, Transgenic ; Molecular Targeted Therapy ; Phosphorylation ; Protein Folding ; Protein Phosphatase 1/*antagonists & inhibitors ; Proteostasis Deficiencies/*drug therapy/*prevention & control ; Signal Transduction
    Print ISSN: 0036-8075
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    Chromosomes. A comprehensive Xist interactome reveals cohesin repulsion and an RNA-directed chromosome conformation (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-06-20
    Description: The inactive X chromosome (Xi) serves as a model to understand gene silencing on a global scale. Here, we perform "identification of direct RNA interacting proteins" (iDRiP) to isolate a comprehensive protein interactome for Xist, an RNA required for Xi silencing. We discover multiple classes of interactors-including cohesins, condensins, topoisomerases, RNA helicases, chromatin remodelers, and modifiers-that synergistically repress Xi transcription. Inhibiting two or three interactors destabilizes silencing. Although Xist attracts some interactors, it repels architectural factors. Xist evicts cohesins from the Xi and directs an Xi-specific chromosome conformation. Upon deleting Xist, the Xi acquires the cohesin-binding and chromosomal architecture of the active X. Our study unveils many layers of Xi repression and demonstrates a central role for RNA in the topological organization of mammalian chromosomes.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Minajigi, Anand -- Froberg, John E -- Wei, Chunyao -- Sunwoo, Hongjae -- Kesner, Barry -- Colognori, David -- Lessing, Derek -- Payer, Bernhard -- Boukhali, Myriam -- Haas, Wilhelm -- Lee, Jeannie T -- R01-DA-38695/DA/NIDA NIH HHS/ -- R03-MH97478/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2015 Jul 17;349(6245). pii: aab2276. doi: 10.1126/science.aab2276. Epub 2015 Jun 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA. ; Massachusetts General Hospital Cancer Center, Charlestown, Boston, MA; Department of Medicine, Harvard Medical School, Boston, MA, USA. ; Howard Hughes Medical Institute; Department of Molecular Biology, Massachusetts General Hospital, Boston, MA, USA; Department of Genetics, Harvard Medical School, Boston, MA, USA. lee@molbio.mgh.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26089354" target="_blank"〉PubMed〈/a〉
    Keywords: Adenosine Triphosphatases/metabolism ; Animals ; Cell Cycle Proteins/*metabolism ; Cells, Cultured ; Chromatin Assembly and Disassembly ; Chromosomal Proteins, Non-Histone/*metabolism ; DNA-Binding Proteins/metabolism ; Embryonic Stem Cells/metabolism ; Fibroblasts/metabolism ; Gene Knockdown Techniques ; Gene Silencing ; Mice ; Multiprotein Complexes/metabolism ; Nucleic Acid Conformation ; Proteomics ; RNA Helicases/metabolism ; RNA, Long Noncoding/*metabolism ; X Chromosome/chemistry/genetics/*metabolism ; *X Chromosome Inactivation
    Print ISSN: 0036-8075
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    Malaria. A forward genetic screen identifies erythrocyte CD55 as essential for Plasmodium falciparum invasion (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-05-09
    Description: Efforts to identify host determinants for malaria have been hindered by the absence of a nucleus in erythrocytes, which precludes genetic manipulation in the cell in which the parasite replicates. We used cultured red blood cells derived from hematopoietic stem cells to carry out a forward genetic screen for Plasmodium falciparum host determinants. We found that CD55 is an essential host factor for P. falciparum invasion. CD55-null erythrocytes were refractory to invasion by all isolates of P. falciparum because parasites failed to attach properly to the erythrocyte surface. Thus, CD55 is an attractive target for the development of malaria therapeutics. Hematopoietic stem cell-based forward genetic screens may be valuable for the identification of additional host determinants of malaria pathogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465434/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4465434/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Egan, Elizabeth S -- Jiang, Rays H Y -- Moechtar, Mischka A -- Barteneva, Natasha S -- Weekes, Michael P -- Nobre, Luis V -- Gygi, Steven P -- Paulo, Joao A -- Frantzreb, Charles -- Tani, Yoshihiko -- Takahashi, Junko -- Watanabe, Seishi -- Goldberg, Jonathan -- Paul, Aditya S -- Brugnara, Carlo -- Root, David E -- Wiegand, Roger C -- Doench, John G -- Duraisingh, Manoj T -- 100140/Wellcome Trust/United Kingdom -- 1K08AI103034-01A1/AI/NIAID NIH HHS/ -- K01 DK098285/DK/NIDDK NIH HHS/ -- K01DK098285/DK/NIDDK NIH HHS/ -- K08 AI103034/AI/NIAID NIH HHS/ -- K12-HD000850/HD/NICHD NIH HHS/ -- R01AI091787/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2015 May 8;348(6235):711-4. doi: 10.1126/science.aaa3526.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, USA. Division of Infectious Diseases, Boston Children's Hospital, Boston, MA, USA. ; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, USA. Department of Global Health and Center for Drug Discovery and Innovation, University of South Florida, Tampa, FL, USA. ; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, USA. ; Department of Pediatrics, Harvard Medical School and Program in Cellular and Molecular Medicine, Boston Children's Hospital, Boston, MA, USA. ; Cambridge Institute for Medical Research, University of Cambridge, Cambridge, UK. ; Department of Cell Biology, Harvard Medical School, Boston, MA, USA. ; Japanese Red Cross Kinki Block Blood Center, Osaka, Japan. ; Japanese Red Cross Kyushu Block Blood Center, Fukuoka, Japan. ; Department of Laboratory Medicine, Boston Children's Hospital and Harvard Medical School, Boston, MA, USA. ; The Broad Institute of Harvard and Massachussetts Insititute of Technology, Cambridge, MA, USAA. ; Department of Immunology and Infectious Diseases, Harvard T. H. Chan School of Public Health, Boston, MA, USA. The Broad Institute of Harvard and Massachussetts Insititute of Technology, Cambridge, MA, USAA. mduraisi@hsph.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25954012" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, CD44/genetics ; Antigens, CD55/*genetics ; Cell Differentiation/genetics ; Cells, Cultured ; Erythrocytes/cytology/metabolism/*parasitology ; Genetic Testing ; Hematopoietic Stem Cells/cytology ; Host-Parasite Interactions/*genetics ; Humans ; Malaria, Falciparum/*genetics/*parasitology ; Plasmodium falciparum/*pathogenicity ; RNA, Small Interfering/genetics
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    HEART DISEASE. Titin mutations in iPS cells define sarcomere insufficiency as a cause of dilated cardiomyopathy (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-09-01
    Description: Human mutations that truncate the massive sarcomere protein titin [TTN-truncating variants (TTNtvs)] are the most common genetic cause for dilated cardiomyopathy (DCM), a major cause of heart failure and premature death. Here we show that cardiac microtissues engineered from human induced pluripotent stem (iPS) cells are a powerful system for evaluating the pathogenicity of titin gene variants. We found that certain missense mutations, like TTNtvs, diminish contractile performance and are pathogenic. By combining functional analyses with RNA sequencing, we explain why truncations in the A-band domain of TTN cause DCM, whereas truncations in the I band are better tolerated. Finally, we demonstrate that mutant titin protein in iPS cell-derived cardiomyocytes results in sarcomere insufficiency, impaired responses to mechanical and beta-adrenergic stress, and attenuated growth factor and cell signaling activation. Our findings indicate that titin mutations cause DCM by disrupting critical linkages between sarcomerogenesis and adaptive remodeling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4618316/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4618316/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hinson, John T -- Chopra, Anant -- Nafissi, Navid -- Polacheck, William J -- Benson, Craig C -- Swist, Sandra -- Gorham, Joshua -- Yang, Luhan -- Schafer, Sebastian -- Sheng, Calvin C -- Haghighi, Alireza -- Homsy, Jason -- Hubner, Norbert -- Church, George -- Cook, Stuart A -- Linke, Wolfgang A -- Chen, Christopher S -- Seidman, J G -- Seidman, Christine E -- EB017103/EB/NIBIB NIH HHS/ -- HG005550/HG/NHGRI NIH HHS/ -- HL007374/HL/NHLBI NIH HHS/ -- HL115553/HL/NHLBI NIH HHS/ -- HL125807/HL/NHLBI NIH HHS/ -- K08 HL125807/HL/NHLBI NIH HHS/ -- T32 HL007208/HL/NHLBI NIH HHS/ -- Department of Health/United Kingdom -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Aug 28;349(6251):982-6. doi: 10.1126/science.aaa5458.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. jthinson@partners.org cseidman@genetics.med.harvard.edu. ; Department of Biomedical Engineering, Boston University, Boston, MA 02215, USA. The Wyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Division of Cardiovascular Medicine, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA. ; Department of Cardiovascular Physiology, Ruhr University Bochum, MA 3/56 D-44780, Bochum, Germany. ; The Wyss Institute for Biologically Inspired Engineering at Harvard University, Boston, MA 02115, USA. Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Cardiovascular and Metabolic Sciences, Max Delbruck Center for Molecular Medicine, Berlin, Germany. ; Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. ; Cardiovascular and Metabolic Sciences, Max Delbruck Center for Molecular Medicine, Berlin, Germany. DZHK (German Center for Cardiovascular Research), Partner Site Berlin, Berlin, Germany. ; National Institute for Health Research (NIHR) Biomedical Research Unit in Cardiovascular Disease at Royal Brompton and Harefield National Health Service (NHS) Foundation Trust, Imperial College London, London, UK. National Heart Centre and Duke-National University, Singapore, Singapore. ; Division of Cardiovascular Medicine, Brigham and Women's Hospital, Boston, MA 02115, USA. Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. Howard Hughes Medical Institute, Chevy Chase, MD 20815, USA. jthinson@partners.org cseidman@genetics.med.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26315439" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenergic beta-Agonists/pharmacology ; Cardiomyopathy, Dilated/*genetics/pathology/*physiopathology ; Cells, Cultured ; Connectin/chemistry/*genetics/*physiology ; Heart Rate ; Humans ; Induced Pluripotent Stem Cells/*physiology ; Isoproterenol/pharmacology ; Mutant Proteins/chemistry/physiology ; *Mutation, Missense ; Myocardial Contraction ; Myocytes, Cardiac/*physiology ; RNA/genetics/metabolism ; Sarcomeres/*physiology/ultrastructure ; Sequence Analysis, RNA ; Signal Transduction ; Stress, Physiological
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    Human oocytes. Error-prone chromosome-mediated spindle assembly favors chromosome segregation defects in human oocytes (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-06-06
    Description: Aneuploidy in human eggs is the leading cause of pregnancy loss and several genetic disorders such as Down syndrome. Most aneuploidy results from chromosome segregation errors during the meiotic divisions of an oocyte, the egg's progenitor cell. The basis for particularly error-prone chromosome segregation in human oocytes is not known. We analyzed meiosis in more than 100 live human oocytes and identified an error-prone chromosome-mediated spindle assembly mechanism as a major contributor to chromosome segregation defects. Human oocytes assembled a meiotic spindle independently of either centrosomes or other microtubule organizing centers. Instead, spindle assembly was mediated by chromosomes and the small guanosine triphosphatase Ran in a process requiring ~16 hours. This unusually long spindle assembly period was marked by intrinsic spindle instability and abnormal kinetochore-microtubule attachments, which favor chromosome segregation errors and provide a possible explanation for high rates of aneuploidy in human eggs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4477045/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4477045/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Holubcova, Zuzana -- Blayney, Martyn -- Elder, Kay -- Schuh, Melina -- MC_U105192711/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2015 Jun 5;348(6239):1143-7. doi: 10.1126/science.aaa9529.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council, Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK. ; Bourn Hall Clinic, Bourn, Cambridge CB23 2TN, UK. ; Medical Research Council, Laboratory of Molecular Biology, Francis Crick Avenue, Cambridge Biomedical Campus, Cambridge CB2 0QH, UK. mschuh@mrc-lmb.cam.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26045437" target="_blank"〉PubMed〈/a〉
    Keywords: Anaphase ; *Aneuploidy ; Animals ; Cells, Cultured ; *Chromosome Segregation ; Female ; Green Fluorescent Proteins/genetics/metabolism ; Humans ; Kinetochores/metabolism ; *Meiosis ; Mice ; Microtubule-Associated Proteins/genetics/metabolism ; Microtubule-Organizing Center/metabolism ; Oocytes/*pathology ; Spindle Apparatus/*metabolism ; ran GTP-Binding Protein/metabolism
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Farm dust and endotoxin protect against allergy through A20 induction in lung epithelial cells (2015)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2015-09-05
    Description: Growing up on a dairy farm protects children from allergy, hay fever, and asthma. A mechanism linking exposure to this endotoxin (bacterial lipopolysaccharide)-rich environment with protection has remained elusive. Here we show that chronic exposure to low-dose endotoxin or farm dust protects mice from developing house dust mite (HDM)-induced asthma. Endotoxin reduced epithelial cell cytokines that activate dendritic cells (DCs), thus suppressing type 2 immunity to HDMs. Loss of the ubiquitin-modifying enzyme A20 in lung epithelium abolished the protective effect. A single-nucleotide polymorphism in the gene encoding A20 was associated with allergy and asthma risk in children growing up on farms. Thus, the farming environment protects from allergy by modifying the communication between barrier epithelial cells and DCs through A20 induction.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schuijs, Martijn J -- Willart, Monique A -- Vergote, Karl -- Gras, Delphine -- Deswarte, Kim -- Ege, Markus J -- Madeira, Filipe Branco -- Beyaert, Rudi -- van Loo, Geert -- Bracher, Franz -- von Mutius, Erika -- Chanez, Pascal -- Lambrecht, Bart N -- Hammad, Hamida -- New York, N.Y. -- Science. 2015 Sep 4;349(6252):1106-10. doi: 10.1126/science.aac6623.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Immunoregulation, VIB Inflammation Research Center, Ghent, Belgium. Department of Internal Medicine, Ghent University, Ghent, Belgium. ; Department of Respiratory Medicine, Assistance Publique Hopitaux de Marseille, UMR INSERM U1067 CNRS 7333, Aix Marseille University, Marseille, France. ; Dr. von Hauner Children's Hospital, Ludwig-Maximilians-Universitat, Munich, Germany. ; Unit of Molecular Signal Transduction, VIB Inflammation Research Center, Ghent, Belgium. Department of Biomedical Molecular Biology, Ghent University, Ghent, Belgium. ; Center for Drug Research, Department of Pharmacy, Ludwig Maximilians University, Butenandtstrasse 5-13, D-81377 Munich, Germany. ; Laboratory of Immunoregulation, VIB Inflammation Research Center, Ghent, Belgium. Department of Internal Medicine, Ghent University, Ghent, Belgium. Department of Pulmonary Medicine, Erasmus Medical Center, Rotterdam, Netherlands. hamida.hammad@ugent.be bart.lambrecht@ugent.be. ; Laboratory of Immunoregulation, VIB Inflammation Research Center, Ghent, Belgium. Department of Internal Medicine, Ghent University, Ghent, Belgium. hamida.hammad@ugent.be bart.lambrecht@ugent.be.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26339029" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Asthma/immunology/prevention & control ; Cells, Cultured ; Child ; DNA-Binding Proteins/*biosynthesis ; Dairying ; Dendritic Cells/immunology ; Dust/*immunology ; Female ; Humans ; Hygiene Hypothesis ; Hypersensitivity/enzymology/immunology/*prevention & control ; Inhalation Exposure ; Intracellular Signaling Peptides and Proteins/*biosynthesis ; Lipopolysaccharides/*immunology ; Lung/*enzymology/immunology ; Mice ; Mice, Inbred C57BL ; Nuclear Proteins/*biosynthesis ; Pyroglyphidae/*immunology ; Respiratory Mucosa/*enzymology/immunology
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    TDP-43 repression of nonconserved cryptic exons is compromised in ALS-FTD (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-08-08
    Description: Cytoplasmic aggregation of TDP-43, accompanied by its nuclear clearance, is a key common pathological hallmark of amyotrophic lateral sclerosis and frontotemporal dementia (ALS-FTD). However, a limited understanding of this RNA-binding protein (RBP) impedes the clarification of pathogenic mechanisms underlying TDP-43 proteinopathy. In contrast to RBPs that regulate splicing of conserved exons, we found that TDP-43 repressed the splicing of nonconserved cryptic exons, maintaining intron integrity. When TDP-43 was depleted from mouse embryonic stem cells, these cryptic exons were spliced into messenger RNAs, often disrupting their translation and promoting nonsense-mediated decay. Moreover, enforced repression of cryptic exons prevented cell death in TDP-43-deficient cells. Furthermore, repression of cryptic exons was impaired in ALS-FTD cases, suggesting that this splicing defect could potentially underlie TDP-43 proteinopathy.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ling, Jonathan P -- Pletnikova, Olga -- Troncoso, Juan C -- Wong, Philip C -- P50AG05146/AG/NIA NIH HHS/ -- New York, N.Y. -- Science. 2015 Aug 7;349(6248):650-5. doi: 10.1126/science.aab0983.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. ; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. ; Department of Pathology, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. Department of Neuroscience, Johns Hopkins University School of Medicine, Baltimore, MD 21205-2196, USA. wong@jhmi.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26250685" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis/*genetics ; Animals ; Base Sequence ; Cells, Cultured ; Cysteine Endopeptidases/genetics ; DNA-Binding Proteins/genetics/*physiology ; Embryonic Stem Cells ; Exons/*genetics ; Frontotemporal Dementia/*genetics ; Gene Knockout Techniques ; HeLa Cells ; Humans ; Mice ; Molecular Sequence Data ; Protein Isoforms/genetics ; *RNA Splicing ; RNA Stability ; RNA, Messenger/metabolism ; Sequence Analysis, DNA
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    Inflammation. Neutrophil extracellular traps license macrophages for cytokine production in atherosclerosis (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-07-18
    Description: Secretion of the cytokine interleukin-1beta (IL-1beta) by macrophages, a major driver of pathogenesis in atherosclerosis, requires two steps: Priming signals promote transcription of immature IL-1beta, and then endogenous "danger" signals activate innate immune signaling complexes called inflammasomes to process IL-1beta for secretion. Although cholesterol crystals are known to act as danger signals in atherosclerosis, what primes IL-1beta transcription remains elusive. Using a murine model of atherosclerosis, we found that cholesterol crystals acted both as priming and danger signals for IL-1beta production. Cholesterol crystals triggered neutrophils to release neutrophil extracellular traps (NETs). NETs primed macrophages for cytokine release, activating T helper 17 (TH17) cells that amplify immune cell recruitment in atherosclerotic plaques. Therefore, danger signals may drive sterile inflammation, such as that seen in atherosclerosis, through their interactions with neutrophils.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Warnatsch, Annika -- Ioannou, Marianna -- Wang, Qian -- Papayannopoulos, Venizelos -- MC_UP_1202/13/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2015 Jul 17;349(6245):316-20. doi: 10.1126/science.aaa8064. Epub 2015 Jul 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Mill Hill Laboratory, Francis Crick Institute, London NW7 1AA, UK. ; Mill Hill Laboratory, Francis Crick Institute, London NW7 1AA, UK. veni.p@crick.ac.uk.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26185250" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Apolipoproteins E/genetics ; Atherosclerosis/*immunology ; Cells, Cultured ; Cholesterol/chemistry/immunology ; Disease Models, Animal ; Extracellular Traps/*immunology ; Humans ; Inflammasomes/immunology ; Inflammation/immunology ; Interleukin-1beta/*biosynthesis/genetics ; Macrophages/*immunology ; Mice ; Mice, Mutant Strains ; Neutrophils/*immunology ; Signal Transduction ; Th17 Cells/immunology ; Transcription, Genetic
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    Proteasomes. A molecular census of 26S proteasomes in intact neurons (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-01-24
    Description: The 26S proteasome is a key player in eukaryotic protein quality control and in the regulation of numerous cellular processes. Here, we describe quantitative in situ structural studies of this highly dynamic molecular machine in intact hippocampal neurons. We used electron cryotomography with the Volta phase plate, which allowed high fidelity and nanometer precision localization of 26S proteasomes. We undertook a molecular census of single- and double-capped proteasomes and assessed the conformational states of individual complexes. Under the conditions of the experiment-that is, in the absence of proteotoxic stress-only 20% of the 26S proteasomes were engaged in substrate processing. The remainder was in the substrate-accepting ground state. These findings suggest that in the absence of stress, the capacity of the proteasome system is not fully used.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Asano, Shoh -- Fukuda, Yoshiyuki -- Beck, Florian -- Aufderheide, Antje -- Forster, Friedrich -- Danev, Radostin -- Baumeister, Wolfgang -- New York, N.Y. -- Science. 2015 Jan 23;347(6220):439-42. doi: 10.1126/science.1261197.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Structural Biology, Max-Planck Institute of Biochemistry, 82152 Martinsried, Germany. ; Department of Molecular Structural Biology, Max-Planck Institute of Biochemistry, 82152 Martinsried, Germany. baumeist@biochem.mpg.de.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25613890" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Hippocampus/*cytology/enzymology ; Neurons/*enzymology/*ultrastructure ; Proteasome Endopeptidase Complex/*chemistry ; Protein Conformation ; Rats ; Stress, Physiological
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    The DNA damage response induces inflammation and senescence by inhibiting autophagy of GATA4 (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-09-26
    Description: Cellular senescence is a terminal stress-activated program controlled by the p53 and p16(INK4a) tumor suppressor proteins. A striking feature of senescence is the senescence-associated secretory phenotype (SASP), a pro-inflammatory response linked to tumor promotion and aging. We have identified the transcription factor GATA4 as a senescence and SASP regulator. GATA4 is stabilized in cells undergoing senescence and is required for the SASP. Normally, GATA4 is degraded by p62-mediated selective autophagy, but this regulation is suppressed during senescence, thereby stabilizing GATA4. GATA4 in turn activates the transcription factor NF-kappaB to initiate the SASP and facilitate senescence. GATA4 activation depends on the DNA damage response regulators ATM and ATR, but not on p53 or p16(INK4a). GATA4 accumulates in multiple tissues, including the aging brain, and could contribute to aging and its associated inflammation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kang, Chanhee -- Xu, Qikai -- Martin, Timothy D -- Li, Mamie Z -- Demaria, Marco -- Aron, Liviu -- Lu, Tao -- Yankner, Bruce A -- Campisi, Judith -- Elledge, Stephen J -- AG009909/AG/NIA NIH HHS/ -- AG017242/AG/NIA NIH HHS/ -- AG046174/AG/NIA NIH HHS/ -- DP1 OD006849/OD/NIH HHS/ -- DP1OD006849/OD/NIH HHS/ -- GM44664/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2015 Sep 25;349(6255):aaa5612. doi: 10.1126/science.aaa5612.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. ; Buck Institute for Research on Aging, Novato, CA 94945, USA. ; Department of Genetics, Harvard Medical School, Boston, MA 02115, USA. ; Department of Genetics, Harvard Medical School, Division of Genetics, Brigham and Women's Hospital, Howard Hughes Medical Institute, Boston, MA 02115, USA. selledge@genetics.med.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26404840" target="_blank"〉PubMed〈/a〉
    Keywords: Aging/*genetics/metabolism ; Animals ; Ataxia Telangiectasia Mutated Proteins/metabolism ; Autophagy/*genetics ; Brain/metabolism ; Cell Aging/*genetics ; Cell Cycle/genetics ; Cells, Cultured ; Cyclin-Dependent Kinase Inhibitor p16 ; *DNA Damage ; Fibroblasts ; GATA4 Transcription Factor/genetics/*metabolism ; Gene Expression Profiling ; Humans ; Inflammation/*genetics ; Interleukin-1alpha/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; MicroRNAs/genetics/metabolism ; NF-kappa B/metabolism ; Phenotype ; Promoter Regions, Genetic ; Tumor Necrosis Factor Receptor-Associated Peptides and ; Proteins/genetics/metabolism ; Tumor Suppressor Protein p53/metabolism
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    Insulin granules. Insulin secretory granules control autophagy in pancreatic beta cells (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-02-24
    Description: Pancreatic beta cells lower insulin release in response to nutrient depletion. The question of whether starved beta cells induce macroautophagy, a predominant mechanism maintaining energy homeostasis, remains poorly explored. We found that, in contrast to many mammalian cells, macroautophagy in pancreatic beta cells was suppressed upon starvation. Instead, starved beta cells induced lysosomal degradation of nascent secretory insulin granules, which was controlled by protein kinase D (PKD), a key player in secretory granule biogenesis. Starvation-induced nascent granule degradation triggered lysosomal recruitment and activation of mechanistic target of rapamycin that suppressed macroautophagy. Switching from macroautophagy to insulin granule degradation was important to keep insulin secretion low upon fasting. Thus, beta cells use a PKD-dependent mechanism to adapt to nutrient availability and couple autophagy flux to secretory function.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Goginashvili, Alexander -- Zhang, Zhirong -- Erbs, Eric -- Spiegelhalter, Coralie -- Kessler, Pascal -- Mihlan, Michael -- Pasquier, Adrien -- Krupina, Ksenia -- Schieber, Nicole -- Cinque, Laura -- Morvan, Joelle -- Sumara, Izabela -- Schwab, Yannick -- Settembre, Carmine -- Ricci, Romeo -- New York, N.Y. -- Science. 2015 Feb 20;347(6224):878-82. doi: 10.1126/science.aaa2628.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institut de Genetique et de Biologie Moleculaire et Cellulaire (IGBMC), INSERM, CNRS, Universite de Strasbourg, 67404 Illkirch, France. ; Cell Biology and Biophysics Unit, European Molecular Biology Laboratory (EMBL), 69117 Heidelberg, Germany. ; Dulbecco Telethon Institute and Telethon Institute of Genetics and Medicine (TIGEM), 80131 Naples, Italy. ; Dulbecco Telethon Institute and Telethon Institute of Genetics and Medicine (TIGEM), 80131 Naples, Italy. Medical Genetics, Department of Medical and Translational Science Unit, Federico II University, Via Pansini 5, 80131 Naples, Italy. ; Institut de Genetique et de Biologie Moleculaire et Cellulaire (IGBMC), INSERM, CNRS, Universite de Strasbourg, 67404 Illkirch, France. Nouvel Hopital Civil, Laboratoire de Biochimie et de Biologie Moleculaire, Universite de Strasbourg, 67091 Strasbourg, France. romeo.ricci@igbmc.fr.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25700520" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autophagy ; Cells, Cultured ; Fasting ; Humans ; Insulin/*secretion ; Insulin-Secreting Cells/*physiology/secretion/ultrastructure ; Mice ; Mice, Mutant Strains ; Mice, Transgenic ; Mitogen-Activated Protein Kinase 13/genetics ; Protein Kinase C/physiology ; Secretory Vesicles/*physiology/secretion
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    Photochemistry. Chemiexcitation of melanin derivatives induces DNA photoproducts long after UV exposure (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-02-24
    Description: Mutations in sunlight-induced melanoma arise from cyclobutane pyrimidine dimers (CPDs), DNA photoproducts that are typically created picoseconds after an ultraviolet (UV) photon is absorbed at thymine or cytosine. We found that in melanocytes, CPDs are generated for 〉3 hours after exposure to UVA, a major component of the radiation in sunlight and in tanning beds. These "dark CPDs" constitute the majority of CPDs and include the cytosine-containing CPDs that initiate UV-signature C--〉T mutations. Dark CPDs arise when UV-induced reactive oxygen and nitrogen species combine to excite an electron in fragments of the pigment melanin. This creates a quantum triplet state that has the energy of a UV photon but induces CPDs by energy transfer to DNA in a radiation-independent manner. Melanin may thus be carcinogenic as well as protective against cancer. These findings also validate the long-standing suggestion that chemically generated excited electronic states are relevant to mammalian biology.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4432913/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4432913/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Premi, Sanjay -- Wallisch, Silvia -- Mano, Camila M -- Weiner, Adam B -- Bacchiocchi, Antonella -- Wakamatsu, Kazumasa -- Bechara, Etelvino J H -- Halaban, Ruth -- Douki, Thierry -- Brash, Douglas E -- 2 P50 CA121974/CA/NCI NIH HHS/ -- P30 DK034989/DK/NIDDK NIH HHS/ -- P30 DK34989/DK/NIDDK NIH HHS/ -- P50 CA121974/CA/NCI NIH HHS/ -- New York, N.Y. -- Science. 2015 Feb 20;347(6224):842-7. doi: 10.1126/science.1256022.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT 06520, USA. ; Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT 06520, USA. Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao Paulo 05513-970 SP, Brazil. ; Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA. ; Department of Chemistry, Fujita Health University School of Health Sciences, Toyoake, Aichi 470-1192, Japan. ; Departamento de Bioquimica, Instituto de Quimica, Universidade de Sao Paulo, Sao Paulo 05513-970 SP, Brazil. Departamento de Ciencias Exatas e da Terra, Universidade Federal de Sao Paulo, Diadema, Sao Paulo 09972-270 SP, Brazil. ; Department of Dermatology, Yale University School of Medicine, New Haven, CT 06520, USA. Yale Comprehensive Cancer Center, Yale University School of Medicine, New Haven, CT 06520, USA. ; INAC/LCIB UMR-E3 CEA-UJF/Commissariat a l'Energie Atomique (CEA), 38054 Grenoble Cedex 9, France. ; Department of Therapeutic Radiology, Yale University School of Medicine, New Haven, CT 06520, USA. Yale Comprehensive Cancer Center, Yale University School of Medicine, New Haven, CT 06520, USA. douglas.brash@yale.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25700512" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Cytosine/metabolism ; DNA/chemistry/genetics/*radiation effects ; DNA Damage/*genetics ; Energy Transfer ; Humans ; Melanins/chemistry/*metabolism ; Melanocytes/metabolism/*radiation effects ; Melanoma/*genetics ; Mice ; Mice, Inbred C57BL ; Mutagenesis ; Mutation ; Neoplasms, Radiation-Induced/*genetics ; Photons ; Pyrimidine Dimers/*metabolism ; Receptor, Melanocortin, Type 1/genetics ; Skin Neoplasms/*genetics ; Sunlight/adverse effects ; Thymine/metabolism ; Ultraviolet Rays
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    Distinct routes of lineage development reshape the human blood hierarchy across ontogeny (2015)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2015-11-07
    Description: In a classical view of hematopoiesis, the various blood cell lineages arise via a hierarchical scheme starting with multipotent stem cells that become increasingly restricted in their differentiation potential through oligopotent and then unipotent progenitors. We developed a cell-sorting scheme to resolve myeloid (My), erythroid (Er), and megakaryocytic (Mk) fates from single CD34(+) cells and then mapped the progenitor hierarchy across human development. Fetal liver contained large numbers of distinct oligopotent progenitors with intermingled My, Er, and Mk fates. However, few oligopotent progenitor intermediates were present in the adult bone marrow. Instead, only two progenitor classes predominate, multipotent and unipotent, with Er-Mk lineages emerging from multipotent cells. The developmental shift to an adult "two-tier" hierarchy challenges current dogma and provides a revised framework to understand normal and disease states of human hematopoiesis.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Notta, Faiyaz -- Zandi, Sasan -- Takayama, Naoya -- Dobson, Stephanie -- Gan, Olga I -- Wilson, Gavin -- Kaufmann, Kerstin B -- McLeod, Jessica -- Laurenti, Elisa -- Dunant, Cyrille F -- McPherson, John D -- Stein, Lincoln D -- Dror, Yigal -- Dick, John E -- Canadian Institutes of Health Research/Canada -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2016 Jan 8;351(6269):aab2116. doi: 10.1126/science.aab2116. Epub 2015 Nov 5.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Princess Margaret Cancer Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada. Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada. ; Princess Margaret Cancer Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada. ; Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada. Ontario Institute for Cancer Research, Toronto, Ontario, Canada. ; Wellcome Trust, Medical Research Council Cambridge Stem Cell Institute, Department of Haematology, University of Cambridge, Cambridge, UK. ; Ecole Polytechnique Federale de Lausanne, LMC, Station 12, Lausanne, CH-1015, Switzerland. ; Medical Biophysics, University of Toronto, Toronto, Ontario, Canada. Ontario Institute for Cancer Research, Toronto, Ontario, Canada. ; The Hospital for Sick Children Research Institute, University of Toronto, Ontario, Canada. ; Princess Margaret Cancer Centre, University Health Network, University of Toronto, Toronto, Ontario, Canada. Department of Molecular Genetics, University of Toronto, Toronto, Ontario, Canada. jdick@uhnres.utoronto.ca.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26541609" target="_blank"〉PubMed〈/a〉
    Keywords: Adult ; Antigens, CD34/analysis ; Cell Lineage/genetics/*physiology ; Cell Separation ; Cells, Cultured ; Erythroid Cells/*cytology ; Fetal Blood/cytology ; Gene Expression Profiling ; Hematopoiesis/genetics/*physiology ; Humans ; Liver/cytology/embryology ; Megakaryocyte Progenitor Cells/*cytology ; Megakaryocytes/*cytology ; Multipotent Stem Cells/cytology ; Myeloid Cells/*cytology ; Transcription, Genetic
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    Generation of compartmentalized pressure by a nuclear piston governs cell motility in a 3D matrix (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-08-30
    Description: Cells use actomyosin contractility to move through three-dimensional (3D) extracellular matrices. Contractility affects the type of protrusions cells use to migrate in 3D, but the mechanisms are unclear. In this work, we found that contractility generated high-pressure lobopodial protrusions in human cells migrating in a 3D matrix. In these cells, the nucleus physically divided the cytoplasm into forward and rear compartments. Actomyosin contractility with the nucleoskeleton-intermediate filament linker protein nesprin-3 pulled the nucleus forward and pressurized the front of the cell. Reducing expression of nesprin-3 decreased and equalized the intracellular pressure. Thus, the nucleus can act as a piston that physically compartmentalizes the cytoplasm and increases the hydrostatic pressure between the nucleus and the leading edge of the cell to drive lamellipodia-independent 3D cell migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Petrie, Ryan J -- Koo, Hyun -- Yamada, Kenneth M -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2014 Aug 29;345(6200):1062-5. doi: 10.1126/science.1256965.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA. petrier@mail.nih.gov kyamada@mail.nih.gov. ; Laboratory of Cell and Developmental Biology, National Institute of Dental and Craniofacial Research, National Institutes of Health, Bethesda, MD 20892-4370, USA. Center for Oral Biology, Department of Microbiology and Immunology, University of Rochester Medical Center, Rochester, NY 14642, USA. Biofilm Research Labs, Levy Center for Oral Health, Department of Orthodontics, University of Pennsylvania School of Dental Medicine, Philadelphia, PA 19104-6030, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25170155" target="_blank"〉PubMed〈/a〉
    Keywords: Actomyosin/physiology ; Cell Movement/*physiology ; Cell Nucleus/*physiology ; Cells, Cultured ; Cytoplasm/physiology ; Extracellular Matrix/*physiology/ultrastructure ; Fibroblasts/*physiology ; Humans ; Hydrostatic Pressure ; Microfilament Proteins ; Pseudopodia/*physiology ; Vimentin/metabolism
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    Highly multiplexed subcellular RNA sequencing in situ (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-03-01
    Description: Understanding the spatial organization of gene expression with single-nucleotide resolution requires localizing the sequences of expressed RNA transcripts within a cell in situ. Here, we describe fluorescent in situ RNA sequencing (FISSEQ), in which stably cross-linked complementary DNA (cDNA) amplicons are sequenced within a biological sample. Using 30-base reads from 8102 genes in situ, we examined RNA expression and localization in human primary fibroblasts with a simulated wound-healing assay. FISSEQ is compatible with tissue sections and whole-mount embryos and reduces the limitations of optical resolution and noisy signals on single-molecule detection. Our platform enables massively parallel detection of genetic elements, including gene transcripts and molecular barcodes, and can be used to investigate cellular phenotype, gene regulation, and environment in situ.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4140943/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4140943/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lee, Je Hyuk -- Daugharthy, Evan R -- Scheiman, Jonathan -- Kalhor, Reza -- Yang, Joyce L -- Ferrante, Thomas C -- Terry, Richard -- Jeanty, Sauveur S F -- Li, Chao -- Amamoto, Ryoji -- Peters, Derek T -- Turczyk, Brian M -- Marblestone, Adam H -- Inverso, Samuel A -- Bernard, Amy -- Mali, Prashant -- Rios, Xavier -- Aach, John -- Church, George M -- GM080177/GM/NIGMS NIH HHS/ -- MH098977/MH/NIMH NIH HHS/ -- P50 HG005550/HG/NHGRI NIH HHS/ -- RC2 HL102815/HL/NHLBI NIH HHS/ -- RC2HL102815/HL/NHLBI NIH HHS/ -- T32 GM007753/GM/NIGMS NIH HHS/ -- T32 GM080177/GM/NIGMS NIH HHS/ -- U01 MH098977/MH/NIMH NIH HHS/ -- New York, N.Y. -- Science. 2014 Mar 21;343(6177):1360-3. doi: 10.1126/science.1250212. Epub 2014 Feb 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Wyss Institute, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24578530" target="_blank"〉PubMed〈/a〉
    Keywords: Base Sequence ; Cell Line ; Cells, Cultured ; DNA, Complementary ; Fluorescence ; Gene Expression Profiling/*methods ; Humans ; Induced Pluripotent Stem Cells ; RNA, Messenger/genetics/metabolism ; Sequence Analysis, RNA/*methods ; Single-Cell Analysis ; Transcription Initiation Site ; *Transcriptome ; Wound Healing
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    Single beta-actin mRNA detection in neurons reveals a mechanism for regulating its translatability (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-01-25
    Description: The physical manifestation of learning and memory formation in the brain can be expressed by strengthening or weakening of synaptic connections through morphological changes. Local actin remodeling underlies some forms of plasticity and may be facilitated by local beta-actin synthesis, but dynamic information is lacking. In this work, we use single-molecule in situ hybridization to demonstrate that dendritic beta-actin messenger RNA (mRNA) and ribosomes are in a masked, neuron-specific form. Chemically induced long-term potentiation prompts transient mRNA unmasking, which depends on factors active during synaptic activity. Ribosomes and single beta-actin mRNA motility increase after stimulation, indicative of release from complexes. Hence, the single-molecule assays we developed allow for the quantification of activity-induced unmasking and availability for active translation. Further, our work demonstrates that beta-actin mRNA and ribosomes are in a masked state that is alleviated by stimulation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121734/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4121734/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buxbaum, Adina R -- Wu, Bin -- Singer, Robert H -- GM84364/GM/NIGMS NIH HHS/ -- NS083085-19/NS/NINDS NIH HHS/ -- R01 NS083085/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Jan 24;343(6169):419-22. doi: 10.1126/science.1242939.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, 1300 Morris Park Avenue, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24458642" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*biosynthesis/genetics ; Animals ; Cells, Cultured ; Dendrites/metabolism ; In Situ Hybridization, Fluorescence/methods ; Long-Term Potentiation/drug effects/*physiology ; Memory/physiology ; Mice ; Mice, Transgenic ; Neuronal Plasticity/drug effects/physiology ; Neurons/*metabolism ; *Protein Biosynthesis ; RNA, Messenger/analysis/*biosynthesis ; RNA, Ribosomal/metabolism ; Ribosomes/*metabolism ; Synapses/metabolism
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    Motor neuron disease. SMN2 splicing modifiers improve motor function and longevity in mice with spinal muscular atrophy (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-08-12
    Description: Spinal muscular atrophy (SMA) is a genetic disease caused by mutation or deletion of the survival of motor neuron 1 (SMN1) gene. A paralogous gene in humans, SMN2, produces low, insufficient levels of functional SMN protein due to alternative splicing that truncates the transcript. The decreased levels of SMN protein lead to progressive neuromuscular degeneration and high rates of mortality. Through chemical screening and optimization, we identified orally available small molecules that shift the balance of SMN2 splicing toward the production of full-length SMN2 messenger RNA with high selectivity. Administration of these compounds to Delta7 mice, a model of severe SMA, led to an increase in SMN protein levels, improvement of motor function, and protection of the neuromuscular circuit. These compounds also extended the life span of the mice. Selective SMN2 splicing modifiers may have therapeutic potential for patients with SMA.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Naryshkin, Nikolai A -- Weetall, Marla -- Dakka, Amal -- Narasimhan, Jana -- Zhao, Xin -- Feng, Zhihua -- Ling, Karen K Y -- Karp, Gary M -- Qi, Hongyan -- Woll, Matthew G -- Chen, Guangming -- Zhang, Nanjing -- Gabbeta, Vijayalakshmi -- Vazirani, Priya -- Bhattacharyya, Anuradha -- Furia, Bansri -- Risher, Nicole -- Sheedy, Josephine -- Kong, Ronald -- Ma, Jiyuan -- Turpoff, Anthony -- Lee, Chang-Sun -- Zhang, Xiaoyan -- Moon, Young-Choon -- Trifillis, Panayiota -- Welch, Ellen M -- Colacino, Joseph M -- Babiak, John -- Almstead, Neil G -- Peltz, Stuart W -- Eng, Loren A -- Chen, Karen S -- Mull, Jesse L -- Lynes, Maureen S -- Rubin, Lee L -- Fontoura, Paulo -- Santarelli, Luca -- Haehnke, Daniel -- McCarthy, Kathleen D -- Schmucki, Roland -- Ebeling, Martin -- Sivaramakrishnan, Manaswini -- Ko, Chien-Ping -- Paushkin, Sergey V -- Ratni, Hasane -- Gerlach, Irene -- Ghosh, Anirvan -- Metzger, Friedrich -- New York, N.Y. -- Science. 2014 Aug 8;345(6197):688-93. doi: 10.1126/science.1250127.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉PTC Therapeutics, 100 Corporate Court, South Plainfield, NJ 07080, USA. ; Section of Neurobiology, Department of Biological Sciences, University of Southern California, Los Angeles, CA 90089, USA. ; PTC Therapeutics, 100 Corporate Court, South Plainfield, NJ 07080, USA. friedrich.metzger@roche.com speltz@ptcbio.com. ; SMA Foundation, 888 Seventh Avenue, Suite 400, New York, NY 10019, USA. ; Department of Stem Cell and Regenerative Biology and the Harvard Stem Cell Institute, Harvard University, Cambridge, MA 02138, USA. ; Roche Pharmaceutical Research and Early Development, Roche Innovation Center Basel, F. Hoffmann-La Roche, Grenzacherstrasse 124, 4070 Basel, Switzerland. ; Roche Pharmaceutical Research and Early Development, Roche Innovation Center Basel, F. Hoffmann-La Roche, Grenzacherstrasse 124, 4070 Basel, Switzerland. friedrich.metzger@roche.com speltz@ptcbio.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25104390" target="_blank"〉PubMed〈/a〉
    Keywords: Administration, Oral ; Alternative Splicing/*drug effects ; Animals ; Cells, Cultured ; Coumarins/*administration & dosage/chemistry ; Disease Models, Animal ; Drug Evaluation, Preclinical ; Humans ; Isocoumarins/*administration & dosage/chemistry ; Longevity/*drug effects ; Mice ; Muscular Atrophy, Spinal/*drug therapy/genetics/metabolism ; Pyrimidinones/*administration & dosage/chemistry ; RNA, Messenger/genetics ; Sequence Deletion ; Small Molecule Libraries/*administration & dosage/chemistry ; Survival of Motor Neuron 2 Protein/*genetics/metabolism
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    Activating hotspot L205R mutation in PRKACA and adrenal Cushing's syndrome (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-04-05
    Description: Adrenal Cushing's syndrome is caused by excess production of glucocorticoid from adrenocortical tumors and hyperplasias, which leads to metabolic disorders. We performed whole-exome sequencing of 49 blood-tumor pairs and RNA sequencing of 44 tumors from cortisol-producing adrenocortical adenomas (ACAs), adrenocorticotropic hormone-independent macronodular adrenocortical hyperplasias (AIMAHs), and adrenocortical oncocytomas (ADOs). We identified a hotspot in the PRKACA gene with a L205R mutation in 69.2% (27 out of 39) of ACAs and validated in 65.5% of a total of 87 ACAs. Our data revealed that the activating L205R mutation, which locates in the P+1 loop of the protein kinase A (PKA) catalytic subunit, promoted PKA substrate phosphorylation and target gene expression. Moreover, we discovered the recurrently mutated gene DOT1L in AIMAHs and CLASP2 in ADOs. Collectively, these data highlight potentially functional mutated genes in adrenal Cushing's syndrome.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cao, Yanan -- He, Minghui -- Gao, Zhibo -- Peng, Ying -- Li, Yanli -- Li, Lin -- Zhou, Weiwei -- Li, Xiangchun -- Zhong, Xu -- Lei, Yiming -- Su, Tingwei -- Wang, Hang -- Jiang, Yiran -- Yang, Lin -- Wei, Wei -- Yang, Xu -- Jiang, Xiuli -- Liu, Li -- He, Juan -- Ye, Junna -- Wei, Qing -- Li, Yingrui -- Wang, Weiqing -- Wang, Jun -- Ning, Guang -- New York, N.Y. -- Science. 2014 May 23;344(6186):913-7. doi: 10.1126/science.1249480. Epub 2014 Apr 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Key Laboratory for Endocrine Tumors, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. ; BGI-Shanghai, BGI-Shenzhen, Shenzhen, China. ; Department of Pathology, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. ; Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Key Laboratory for Endocrine Tumors, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. guangning@medmail.com.cn wangj@genomics.org.cn wqingw@hotmail.com. ; BGI-Shanghai, BGI-Shenzhen, Shenzhen, China. Department of Biology, University of Copenhagen, Copenhagen, Denmark. King Abdulaziz University, Jeddah, Saudi Arabia. Macau University of Science and Technology, Macau, China. Department of Medicine, University of Hong Kong, Hong Kong. guangning@medmail.com.cn wangj@genomics.org.cn wqingw@hotmail.com. ; Shanghai Clinical Center for Endocrine and Metabolic Diseases, Shanghai Key Laboratory for Endocrine Tumors, Rui-Jin Hospital, Shanghai Jiao-Tong University School of Medicine, Shanghai, China. Laboratory of Endocrinology and Metabolism, Institute of Health Sciences, Shanghai Institutes for Biological Sciences (SIBS), Chinese Academy of Sciences (CAS), and Shanghai Jiao Tong University School of Medicine (SJTUSM), Shanghai, China. guangning@medmail.com.cn wangj@genomics.org.cn wqingw@hotmail.com.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24700472" target="_blank"〉PubMed〈/a〉
    Keywords: Adrenal Cortex Neoplasms/*genetics/*metabolism ; Adrenocortical Adenoma/*genetics/*metabolism ; Amino Acid Substitution ; Arginine/genetics ; Catalytic Domain/genetics ; Cells, Cultured ; Cushing Syndrome/*genetics ; Cyclic AMP-Dependent Protein Kinase Catalytic Subunits/chemistry/*genetics ; Glucocorticoids/metabolism ; Humans ; Hydrocortisone/*metabolism ; Leucine/genetics ; Methyltransferases/genetics ; Microtubule-Associated Proteins/genetics ; Mutation
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    Poly-dipeptides encoded by the C9orf72 repeats bind nucleoli, impede RNA biogenesis, and kill cells (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-08-02
    Description: Many RNA regulatory proteins controlling pre-messenger RNA splicing contain serine:arginine (SR) repeats. Here, we found that these SR domains bound hydrogel droplets composed of fibrous polymers of the low-complexity domain of heterogeneous ribonucleoprotein A2 (hnRNPA2). Hydrogel binding was reversed upon phosphorylation of the SR domain by CDC2-like kinases 1 and 2 (CLK1/2). Mutated variants of the SR domains changing serine to glycine (SR-to-GR variants) also bound to hnRNPA2 hydrogels but were not affected by CLK1/2. When expressed in mammalian cells, these variants bound nucleoli. The translation products of the sense and antisense transcripts of the expansion repeats associated with the C9orf72 gene altered in neurodegenerative disease encode GRn and PRn repeat polypeptides. Both peptides bound to hnRNPA2 hydrogels independent of CLK1/2 activity. When applied to cultured cells, both peptides entered cells, migrated to the nucleus, bound nucleoli, and poisoned RNA biogenesis, which caused cell death.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459787/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4459787/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kwon, Ilmin -- Xiang, Siheng -- Kato, Masato -- Wu, Leeju -- Theodoropoulos, Pano -- Wang, Tao -- Kim, Jiwoong -- Yun, Jonghyun -- Xie, Yang -- McKnight, Steven L -- U01 GM107623/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2014 Sep 5;345(6201):1139-45. doi: 10.1126/science.1254917. Epub 2014 Jul 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA. ; Quantitative Biomedical Research Center, Department of Clinical Sciences, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA. ; Department of Biochemistry, UT Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, TX 75390-9152, USA. steven.mcknight@utsouthwestern.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25081482" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Amyotrophic Lateral Sclerosis/genetics/*metabolism/pathology ; Astrocytes/*metabolism/pathology ; Cell Death ; Cell Nucleolus/*metabolism ; Cells, Cultured ; Dipeptides/genetics/*metabolism/pharmacology ; Frontotemporal Dementia/genetics/*metabolism/pathology ; Glutamate Plasma Membrane Transport Proteins/genetics ; Heterogeneous-Nuclear Ribonucleoprotein Group A-B/*metabolism ; Humans ; Hydrogel ; Phosphorylation ; Protein Biosynthesis ; Protein Structure, Tertiary ; Protein-Serine-Threonine Kinases/metabolism ; Protein-Tyrosine Kinases/metabolism ; Proteins/*genetics ; RNA, Antisense/antagonists & inhibitors/biosynthesis ; RNA, Messenger/antagonists & inhibitors/biosynthesis ; RNA, Ribosomal/antagonists & inhibitors/biosynthesis ; Repetitive Sequences, Amino Acid ; Transcription, Genetic
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    Virus entry. Lassa virus entry requires a trigger-induced receptor switch (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-06-28
    Description: Lassa virus spreads from a rodent to humans and can lead to lethal hemorrhagic fever. Despite its broad tropism, chicken cells were reported 30 years ago to resist infection. We found that Lassa virus readily engaged its cell-surface receptor alpha-dystroglycan in avian cells, but virus entry in susceptible species involved a pH-dependent switch to an intracellular receptor, the lysosome-resident protein LAMP1. Iterative haploid screens revealed that the sialyltransferase ST3GAL4 was required for the interaction of the virus glycoprotein with LAMP1. A single glycosylated residue in LAMP1, present in susceptible species but absent in birds, was essential for interaction with the Lassa virus envelope protein and subsequent infection. The resistance of Lamp1-deficient mice to Lassa virus highlights the relevance of this receptor switch in vivo.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239993/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4239993/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Jae, Lucas T -- Raaben, Matthijs -- Herbert, Andrew S -- Kuehne, Ana I -- Wirchnianski, Ariel S -- Soh, Timothy K -- Stubbs, Sarah H -- Janssen, Hans -- Damme, Markus -- Saftig, Paul -- Whelan, Sean P -- Dye, John M -- Brummelkamp, Thijn R -- AI081842/AI/NIAID NIH HHS/ -- AI109740/AI/NIAID NIH HHS/ -- R01 AI081842/AI/NIAID NIH HHS/ -- T32 AI007245/AI/NIAID NIH HHS/ -- U19 AI109740/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Jun 27;344(6191):1506-10. doi: 10.1126/science.1252480.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, Netherlands. ; Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, Netherlands. Department of Microbiology and Immunobiology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. ; U.S. Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, MD 21702-5011, USA. ; Department of Microbiology and Immunobiology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. ; Biochemisches Institut, Christian Albrechts-Universitat Kiel, 24118 Kiel, Germany. ; Department of Microbiology and Immunobiology, Harvard Medical School, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. t.brummelkamp@nki.nl john.m.dye1.civ@mail.mil sean_whelan@hms.harvard.edu. ; U.S. Army Medical Research Institute of Infectious Diseases, 1425 Porter Street, Fort Detrick, MD 21702-5011, USA. t.brummelkamp@nki.nl john.m.dye1.civ@mail.mil sean_whelan@hms.harvard.edu. ; Netherlands Cancer Institute, Plesmanlaan 121, 1066 CX, Amsterdam, Netherlands. CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090 Vienna, Austria. Cancer Genomics Center (CGC.nl), Plesmanlaan 121, 1066 CX, Amsterdam, Netherlands. t.brummelkamp@nki.nl john.m.dye1.civ@mail.mil sean_whelan@hms.harvard.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24970085" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Cell Membrane/metabolism/virology ; Cells, Cultured ; Chickens ; Dystroglycans/genetics/metabolism ; Glycosylation ; Humans ; Hydrogen-Ion Concentration ; Lassa Fever/virology ; Lassa virus/*physiology ; Lysosomal-Associated Membrane Protein 1/chemistry/*metabolism ; Lysosomes/metabolism/virology ; Mice ; Mice, Knockout ; Molecular Sequence Data ; Protein Binding ; Receptors, Virus/*metabolism ; Sialyltransferases/metabolism ; Viral Envelope Proteins/*metabolism ; *Virus Internalization
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    Visualization of dynamics of single endogenous mRNA labeled in live mouse (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-01-25
    Description: The transcription and transport of messenger RNA (mRNA) are critical steps in regulating the spatial and temporal components of gene expression, but it has not been possible to observe the dynamics of endogenous mRNA in primary mammalian tissues. We have developed a transgenic mouse in which all beta-actin mRNA is fluorescently labeled. We found that beta-actin mRNA in primary fibroblasts localizes predominantly by diffusion and trapping as single mRNAs. In cultured neurons and acute brain slices, we found that multiple beta-actin mRNAs can assemble together, travel by active transport, and disassemble upon depolarization by potassium chloride. Imaging of brain slices revealed immediate early induction of beta-actin transcription after depolarization. Studying endogenous mRNA in live mouse tissues provides insight into its dynamic regulation within the context of the cellular and tissue microenvironment.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4111226/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4111226/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Park, Hye Yoon -- Lim, Hyungsik -- Yoon, Young J -- Follenzi, Antonia -- Nwokafor, Chiso -- Lopez-Jones, Melissa -- Meng, Xiuhua -- Singer, Robert H -- EB13571/EB/NIBIB NIH HHS/ -- F32-GM87122/GM/NIGMS NIH HHS/ -- GM84364/GM/NIGMS NIH HHS/ -- NS083085-19/NS/NINDS NIH HHS/ -- R01 EB013571/EB/NIBIB NIH HHS/ -- R01 NS083085/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2014 Jan 24;343(6169):422-4. doi: 10.1126/science.1239200.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Anatomy and Structural Biology, Albert Einstein College of Medicine, Bronx, NY 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24458643" target="_blank"〉PubMed〈/a〉
    Keywords: Actins/*biosynthesis/genetics ; Animals ; Brain/cytology/metabolism ; Cells, Cultured ; Fibroblasts/metabolism ; Fluorescent Dyes/chemistry ; Mice ; Mice, Transgenic ; Neuroimaging/*methods ; Neurons/metabolism ; Protein Biosynthesis ; RNA, Messenger/analysis/biosynthesis/*metabolism ; Staining and Labeling
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    Interferon-lambda cures persistent murine norovirus infection in the absence of adaptive immunity (2014)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2014-11-29
    Description: Norovirus gastroenteritis is a major public health burden worldwide. Although fecal shedding is important for transmission of enteric viruses, little is known about the immune factors that restrict persistent enteric infection. We report here that although the cytokines interferon-alpha (IFN-alpha) and IFN-beta prevented the systemic spread of murine norovirus (MNoV), only IFN-lambda controlled persistent enteric infection. Infection-dependent induction of IFN-lambda was governed by the MNoV capsid protein and correlated with diminished enteric persistence. Treatment of established infection with IFN-lambda cured mice in a manner requiring nonhematopoietic cell expression of the IFN-lambda receptor, Ifnlr1, and independent of adaptive immunity. These results suggest the therapeutic potential of IFN-lambda for curing virus infections in the gastrointestinal tract.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398891/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4398891/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nice, Timothy J -- Baldridge, Megan T -- McCune, Broc T -- Norman, Jason M -- Lazear, Helen M -- Artyomov, Maxim -- Diamond, Michael S -- Virgin, Herbert W -- 5T32A100716334/PHS HHS/ -- 5T32AI007163/AI/NIAID NIH HHS/ -- 5T32CA009547/CA/NCI NIH HHS/ -- F31 CA177194/CA/NCI NIH HHS/ -- F31CA177194-01/CA/NCI NIH HHS/ -- R01 AI084887/AI/NIAID NIH HHS/ -- T32 AI007163/AI/NIAID NIH HHS/ -- T32 CA009547/CA/NCI NIH HHS/ -- U19 AI083019/AI/NIAID NIH HHS/ -- U19 AI106772/AI/NIAID NIH HHS/ -- U19 AI109725/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2015 Jan 16;347(6219):269-73. doi: 10.1126/science.1258100. Epub 2014 Nov 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Medicine, Washington University School of Medicine, St. Louis, MO 63110, USA. Department of Molecular Microbiology, Washington University School of Medicine, St. Louis, MO 63110, USA. ; Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA. virgin@wustl.edu.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25431489" target="_blank"〉PubMed〈/a〉
    Keywords: Adaptive Immunity ; Animals ; Caliciviridae Infections/*drug therapy/*immunology/virology ; Capsid Proteins/immunology/metabolism ; Cells, Cultured ; Cytokines/biosynthesis/*immunology/*therapeutic use ; Feces/virology ; Gastroenteritis/drug therapy/*immunology/virology ; Immunity, Innate ; Interferon-alpha/biosynthesis/immunology ; Interferon-beta/biosynthesis/immunology ; Mice ; Mice, Inbred C57BL ; Norovirus/*immunology/*physiology ; Virus Replication ; Virus Shedding
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    T cell immunity. Functional heterogeneity of human memory CD4(+) T cell clones primed by pathogens or vaccines (2014)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2014-12-06
    Description: Distinct types of CD4(+) T cells protect the host against different classes of pathogens. However, it is unclear whether a given pathogen induces a single type of polarized T cell. By combining antigenic stimulation and T cell receptor deep sequencing, we found that human pathogen- and vaccine-specific T helper 1 (T(H)1), T(H)2, and T(H)17 memory cells have different frequencies but comparable diversity and comprise not only clones polarized toward a single fate, but also clones whose progeny have acquired multiple fates. Single naive T cells primed by a pathogen in vitro could also give rise to multiple fates. Our results unravel an unexpected degree of interclonal and intraclonal functional heterogeneity of the human T cell response and suggest that polarized responses result from preferential expansion rather than priming.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Becattini, Simone -- Latorre, Daniela -- Mele, Federico -- Foglierini, Mathilde -- De Gregorio, Corinne -- Cassotta, Antonino -- Fernandez, Blanca -- Kelderman, Sander -- Schumacher, Ton N -- Corti, Davide -- Lanzavecchia, Antonio -- Sallusto, Federica -- New York, N.Y. -- Science. 2015 Jan 23;347(6220):400-6. doi: 10.1126/science.1260668. Epub 2014 Dec 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Research in Biomedicine, Bellinzona, Universita della Svizzera Italiana, Lugano, Switzerland. Institute of Microbiology, ETH Zurich, Zurich, Switzerland. ; Institute for Research in Biomedicine, Bellinzona, Universita della Svizzera Italiana, Lugano, Switzerland. ; Division of Immunology, Netherlands Cancer Institute, Amsterdam, Netherlands. ; Institute for Research in Biomedicine, Bellinzona, Universita della Svizzera Italiana, Lugano, Switzerland. federica.sallusto@irb.usi.ch.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25477212" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; CD4-Positive T-Lymphocytes/*immunology ; Candida albicans/*immunology ; Cells, Cultured ; Clone Cells ; High-Throughput Nucleotide Sequencing ; Host-Pathogen Interactions/*immunology ; Humans ; *Immunologic Memory ; Lymphocyte Activation ; Molecular Sequence Data ; Mycobacterium tuberculosis/*immunology ; Receptors, Antigen, T-Cell/genetics ; T-Lymphocyte Subsets/*immunology ; Th1 Cells/immunology ; Th17 Cells/immunology ; Th2 Cells/immunology ; Vaccines/*immunology
    Print ISSN: 0036-8075
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    Interfollicular epidermal stem cells self-renew via autocrine Wnt signaling (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-12-07
    Description: The skin is a classical example of a tissue maintained by stem cells. However, the identity of the stem cells that maintain the interfollicular epidermis and the source of the signals that control their activity remain unclear. Using mouse lineage tracing and quantitative clonal analyses, we showed that the Wnt target gene Axin2 marks interfollicular epidermal stem cells. These Axin2-expressing cells constitute the majority of the basal epidermal layer, compete neutrally, and require Wnt/beta-catenin signaling to proliferate. The same cells contribute robustly to wound healing, with no requirement for a quiescent stem cell subpopulation. By means of double-labeling RNA in situ hybridization in mice, we showed that the Axin2-expressing cells themselves produce Wnt signals as well as long-range secreted Wnt inhibitors, suggesting an autocrine mechanism of stem cell self-renewal.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4081860/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4081860/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lim, Xinhong -- Tan, Si Hui -- Koh, Winston Lian Chye -- Chau, Rosanna Man Wah -- Yan, Kelley S -- Kuo, Calvin J -- van Amerongen, Renee -- Klein, Allon Moshe -- Nusse, Roel -- 1R01DK085720/DK/NIDDK NIH HHS/ -- 1U01DK085527/DK/NIDDK NIH HHS/ -- 5K08DK096048/DK/NIDDK NIH HHS/ -- K08 DK096048/DK/NIDDK NIH HHS/ -- P30 DK026743/DK/NIDDK NIH HHS/ -- R01 DK085720/DK/NIDDK NIH HHS/ -- U01 DK085527/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1226-30. doi: 10.1126/science.1239730.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Howard Hughes Medical Institute (HHMI), Institute for Stem Cell Biology and Regenerative Medicine, School of Medicine, Stanford University, Stanford, CA, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311688" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Autocrine Communication ; Axin Protein/genetics/metabolism ; Cell Differentiation ; Cell Lineage ; Cell Proliferation ; Cells, Cultured ; Epidermis/*cytology/injuries/metabolism ; Epithelial Cells/cytology/metabolism ; Gene Expression ; Homeostasis ; Humans ; Intercellular Signaling Peptides and Proteins/metabolism ; Keratinocytes/cytology/metabolism ; Mice ; Regeneration ; Skin/injuries ; Stem Cell Niche ; Stem Cells/cytology/*physiology ; Wnt Proteins/metabolism ; *Wnt Signaling Pathway ; Wound Healing ; beta Catenin/genetics/metabolism
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    B cells use mechanical energy to discriminate antigen affinities (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-05-21
    Description: The generation of high-affinity antibodies depends on the ability of B cells to extract antigens from the surfaces of antigen-presenting cells. B cells that express high-affinity B cell receptors (BCRs) acquire more antigen and obtain better T cell help. However, the mechanisms by which B cells extract antigen remain unclear. Using fluid and flexible membrane substrates to mimic antigen-presenting cells, we showed that B cells acquire antigen by dynamic myosin IIa-mediated contractions that pull out and invaginate the presenting membranes. The forces generated by myosin IIa contractions ruptured most individual BCR-antigen bonds and promoted internalization of only high-affinity, multivalent BCR microclusters. Thus, B cell contractility contributes to affinity discrimination by mechanically testing the strength of antigen binding.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3713314/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3713314/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Natkanski, Elizabeth -- Lee, Wing-Yiu -- Mistry, Bhakti -- Casal, Antonio -- Molloy, Justin E -- Tolar, Pavel -- MC_U117570592/Medical Research Council/United Kingdom -- MC_U117597138/Medical Research Council/United Kingdom -- U117570592/Medical Research Council/United Kingdom -- U117597138/Medical Research Council/United Kingdom -- New York, N.Y. -- Science. 2013 Jun 28;340(6140):1587-90. doi: 10.1126/science.1237572. Epub 2013 May 16.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Immune Cell Biology, MRC National Institute for Medical Research, Mill Hill, London NW7 1AA, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23686338" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antibody Affinity ; *Antigen Presentation ; Antigens/*immunology ; B-Lymphocytes/*immunology ; Cells, Cultured ; Mechanical Processes ; Mice ; Mice, Inbred C57BL ; Microscopy, Atomic Force ; Nonmuscle Myosin Type IIA/*physiology ; Receptors, Antigen, B-Cell/immunology
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    Targeted inhibition of mutant IDH2 in leukemia cells induces cellular differentiation (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-04-06
    Description: A number of human cancers harbor somatic point mutations in the genes encoding isocitrate dehydrogenases 1 and 2 (IDH1 and IDH2). These mutations alter residues in the enzyme active sites and confer a gain-of-function in cancer cells, resulting in the accumulation and secretion of the oncometabolite (R)-2-hydroxyglutarate (2HG). We developed a small molecule, AGI-6780, that potently and selectively inhibits the tumor-associated mutant IDH2/R140Q. A crystal structure of AGI-6780 complexed with IDH2/R140Q revealed that the inhibitor binds in an allosteric manner at the dimer interface. The results of steady-state enzymology analysis were consistent with allostery and slow-tight binding by AGI-6780. Treatment with AGI-6780 induced differentiation of TF-1 erythroleukemia and primary human acute myelogenous leukemia cells in vitro. These data provide proof-of-concept that inhibitors targeting mutant IDH2/R140Q could have potential applications as a differentiation therapy for cancer.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Fang -- Travins, Jeremy -- DeLaBarre, Byron -- Penard-Lacronique, Virginie -- Schalm, Stefanie -- Hansen, Erica -- Straley, Kimberly -- Kernytsky, Andrew -- Liu, Wei -- Gliser, Camelia -- Yang, Hua -- Gross, Stefan -- Artin, Erin -- Saada, Veronique -- Mylonas, Elena -- Quivoron, Cyril -- Popovici-Muller, Janeta -- Saunders, Jeffrey O -- Salituro, Francesco G -- Yan, Shunqi -- Murray, Stuart -- Wei, Wentao -- Gao, Yi -- Dang, Lenny -- Dorsch, Marion -- Agresta, Sam -- Schenkein, David P -- Biller, Scott A -- Su, Shinsan M -- de Botton, Stephane -- Yen, Katharine E -- New York, N.Y. -- Science. 2013 May 3;340(6132):622-6. doi: 10.1126/science.1234769. Epub 2013 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Agios Pharmaceuticals, Cambridge, MA 02139-4169, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23558173" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Site ; Antineoplastic Agents/chemistry/metabolism/pharmacology ; Catalytic Domain ; Cell Line, Tumor ; Cell Proliferation ; Cells, Cultured ; Crystallography, X-Ray ; Enzyme Inhibitors/chemistry/metabolism/*pharmacology ; Erythropoiesis/drug effects ; Gene Expression Regulation, Leukemic ; Glutarates/metabolism ; Hematopoiesis/*drug effects ; Humans ; Isocitrate Dehydrogenase/*antagonists & inhibitors/chemistry/*genetics/metabolism ; Leukemia, Erythroblastic, Acute ; Leukemia, Myeloid, Acute/drug therapy/*enzymology/genetics/pathology ; Molecular Targeted Therapy ; Mutant Proteins/antagonists & inhibitors/chemistry/metabolism ; Phenylurea Compounds/chemistry/metabolism/*pharmacology ; Point Mutation ; Protein Multimerization ; Protein Structure, Secondary ; Small Molecule Libraries ; Sulfonamides/chemistry/metabolism/*pharmacology
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    Erythropoietin derived by chemical synthesis (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-18
    Description: Erythropoietin is a signaling glycoprotein that controls the fundamental process of erythropoiesis, orchestrating the production and maintenance of red blood cells. As administrated clinically, erythropoietin has a polypeptide backbone with complex dishomogeneity in its carbohydrate domains. Here we describe the total synthesis of homogeneous erythropoietin with consensus carbohydrate domains incorporated at all of the native glycosylation sites. The oligosaccharide sectors were built by total synthesis and attached stereospecifically to peptidyl fragments of the wild-type primary sequence, themselves obtained by solid-phase peptide synthesis. The glycopeptidyl constructs were joined by chemical ligation, followed by metal-free dethiylation, and subsequently folded. This homogeneous erythropoietin glycosylated at the three wild-type aspartates with N-linked high-mannose sialic acid-containing oligosaccharides and O-linked glycophorin exhibits Procrit-level in vivo activity in mice.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4080428/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4080428/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Wang, Ping -- Dong, Suwei -- Shieh, Jae-Hung -- Peguero, Elizabeth -- Hendrickson, Ronald -- Moore, Malcolm A S -- Danishefsky, Samuel J -- HL025848/HL/NHLBI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 GM109760/GM/NIGMS NIH HHS/ -- R01 HL025848/HL/NHLBI NIH HHS/ -- New York, N.Y. -- Science. 2013 Dec 13;342(6164):1357-60. doi: 10.1126/science.1245095.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Bioorganic Chemistry, Sloan-Kettering Institute for Cancer Research, 1275 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24337294" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Aspartic Acid/chemistry ; Cells, Cultured ; Consensus Sequence ; Dose-Response Relationship, Drug ; Erythrocyte Count ; Erythropoietin/*administration & dosage/*chemical synthesis/chemistry ; Glycophorin/chemistry ; Glycosylation ; Injections, Subcutaneous ; Mannose/chemistry ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; N-Acetylneuraminic Acid/chemistry ; Oligosaccharides/chemistry ; Reticulocytes/drug effects
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    An erythroid enhancer of BCL11A subject to genetic variation determines fetal hemoglobin level (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-10-12
    Description: Genome-wide association studies (GWASs) have ascertained numerous trait-associated common genetic variants, frequently localized to regulatory DNA. We found that common genetic variation at BCL11A associated with fetal hemoglobin (HbF) level lies in noncoding sequences decorated by an erythroid enhancer chromatin signature. Fine-mapping uncovers a motif-disrupting common variant associated with reduced transcription factor (TF) binding, modestly diminished BCL11A expression, and elevated HbF. The surrounding sequences function in vivo as a developmental stage-specific, lineage-restricted enhancer. Genome engineering reveals the enhancer is required in erythroid but not B-lymphoid cells for BCL11A expression. These findings illustrate how GWASs may expose functional variants of modest impact within causal elements essential for appropriate gene expression. We propose the GWAS-marked BCL11A enhancer represents an attractive target for therapeutic genome engineering for the beta-hemoglobinopathies.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4018826/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4018826/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Bauer, Daniel E -- Kamran, Sophia C -- Lessard, Samuel -- Xu, Jian -- Fujiwara, Yuko -- Lin, Carrie -- Shao, Zhen -- Canver, Matthew C -- Smith, Elenoe C -- Pinello, Luca -- Sabo, Peter J -- Vierstra, Jeff -- Voit, Richard A -- Yuan, Guo-Cheng -- Porteus, Matthew H -- Stamatoyannopoulos, John A -- Lettre, Guillaume -- Orkin, Stuart H -- 123382/Canadian Institutes of Health Research/Canada -- K08 DK093705/DK/NIDDK NIH HHS/ -- K08DK093705/DK/NIDDK NIH HHS/ -- P01HL032262/HL/NHLBI NIH HHS/ -- P30 DK049216/DK/NIDDK NIH HHS/ -- P30DK049216/DK/NIDDK NIH HHS/ -- R01 HG005085/HG/NHGRI NIH HHS/ -- R01 HL032259/HL/NHLBI NIH HHS/ -- R01HL032259/HL/NHLBI NIH HHS/ -- U54HG004594/HG/NHGRI NIH HHS/ -- U54HG007010/HG/NHGRI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Oct 11;342(6155):253-7. doi: 10.1126/science.1242088.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Hematology/Oncology, Boston Children's Hospital, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24115442" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Carrier Proteins/*genetics ; Cell Line, Tumor ; Cells, Cultured ; Chromatin/genetics/metabolism ; Chromatin Immunoprecipitation ; Chromosome Mapping ; *Enhancer Elements, Genetic ; Erythroid Cells/*metabolism ; Fetal Hemoglobin/*biosynthesis/genetics ; *Gene Expression Regulation ; Gene Targeting ; Genetic Engineering ; Genetic Variation ; Genome-Wide Association Study ; Hemoglobinopathies/*genetics/therapy ; Humans ; Mice ; Nuclear Proteins/*genetics ; Precursor Cells, B-Lymphoid/metabolism ; Transcription Factors/genetics/metabolism
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    Mice genetically deficient in vasopressin V1a and V1b receptors are resistant to jet lag (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-10-05
    Description: Jet-lag symptoms arise from temporal misalignment between the internal circadian clock and external solar time. We found that circadian rhythms of behavior (locomotor activity), clock gene expression, and body temperature immediately reentrained to phase-shifted light-dark cycles in mice lacking vasopressin receptors V1a and V1b (V1a(-/-)V1b(-/-)). Nevertheless, the behavior of V1a(-/-)V1b(-/-) mice was still coupled to the internal clock, which oscillated normally under standard conditions. Experiments with suprachiasmatic nucleus (SCN) slices in culture suggested that interneuronal communication mediated by V1a and V1b confers on the SCN an intrinsic resistance to external perturbation. Pharmacological blockade of V1a and V1b in the SCN of wild-type mice resulted in accelerated recovery from jet lag, which highlights the potential of vasopressin signaling as a therapeutic target for management of circadian rhythm misalignment, such as jet lag and shift work.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamaguchi, Yoshiaki -- Suzuki, Toru -- Mizoro, Yasutaka -- Kori, Hiroshi -- Okada, Kazuki -- Chen, Yulin -- Fustin, Jean-Michel -- Yamazaki, Fumiyoshi -- Mizuguchi, Naoki -- Zhang, Jing -- Dong, Xin -- Tsujimoto, Gozoh -- Okuno, Yasushi -- Doi, Masao -- Okamura, Hitoshi -- New York, N.Y. -- Science. 2013 Oct 4;342(6154):85-90. doi: 10.1126/science.1238599.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Systems Biology, Graduate School of Pharmaceutical Sciences, Kyoto University, Sakyo-ku, Kyoto 606-8501, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24092737" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antidiuretic Hormone Receptor Antagonists ; Body Temperature/genetics ; CLOCK Proteins/genetics ; Cell Communication/drug effects/genetics ; Cells, Cultured ; Circadian Rhythm/genetics ; Gene Expression Regulation ; Jet Lag Syndrome/*genetics/physiopathology ; Mice ; Mice, Knockout ; Motor Activity/genetics ; Receptors, Vasopressin/*genetics ; Suprachiasmatic Nucleus/physiopathology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    53BP1 regulates DSB repair using Rif1 to control 5' end resection (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-01-12
    Description: The choice between double-strand break (DSB) repair by either homology-directed repair (HDR) or nonhomologous end joining (NHEJ) is tightly regulated. Defects in this regulation can induce genome instability and cancer. 53BP1 is critical for the control of DSB repair, promoting NHEJ, and inhibiting the 5' end resection needed for HDR. Using dysfunctional telomeres and genome-wide DSBs, we identify Rif1 as the main factor used by 53BP1 to impair 5' end resection. Rif1 inhibits resection involving CtIP, BLM, and Exo1; limits accumulation of BRCA1/BARD1 complexes at sites of DNA damage; and defines one of the mechanisms by which 53BP1 causes chromosomal abnormalities in Brca1-deficient cells. These data establish Rif1 as an important contributor to the control of DSB repair by 53BP1.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3664841/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3664841/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zimmermann, Michal -- Lottersberger, Francisca -- Buonomo, Sara B -- Sfeir, Agnel -- de Lange, Titia -- R37 GM049046/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 8;339(6120):700-4. doi: 10.1126/science.1231573. Epub 2013 Jan 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23306437" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; BRCA1 Protein/metabolism ; Cells, Cultured ; Chromosomal Proteins, Non-Histone/chemistry/genetics/*metabolism ; DNA/metabolism ; *DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; *DNA Repair ; DNA-Binding Proteins/chemistry/genetics/*metabolism ; Mice ; Replication Protein A/metabolism ; Telomere/*metabolism ; Telomere-Binding Proteins/*metabolism ; Telomeric Repeat Binding Protein 2/genetics/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Rif1 prevents resection of DNA breaks and promotes immunoglobulin class switching (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-01-12
    Description: DNA double-strand breaks (DSBs) represent a threat to the genome because they can lead to the loss of genetic information and chromosome rearrangements. The DNA repair protein p53 binding protein 1 (53BP1) protects the genome by limiting nucleolytic processing of DSBs by a mechanism that requires its phosphorylation, but whether 53BP1 does so directly is not known. Here, we identify Rap1-interacting factor 1 (Rif1) as an ATM (ataxia-telangiectasia mutated) phosphorylation-dependent interactor of 53BP1 and show that absence of Rif1 results in 5'-3' DNA-end resection in mice. Consistent with enhanced DNA resection, Rif1 deficiency impairs DNA repair in the G(1) and S phases of the cell cycle, interferes with class switch recombination in B lymphocytes, and leads to accumulation of chromosome DSBs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815530/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3815530/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Di Virgilio, Michela -- Callen, Elsa -- Yamane, Arito -- Zhang, Wenzhu -- Jankovic, Mila -- Gitlin, Alexander D -- Feldhahn, Niklas -- Resch, Wolfgang -- Oliveira, Thiago Y -- Chait, Brian T -- Nussenzweig, Andre -- Casellas, Rafael -- Robbiani, Davide F -- Nussenzweig, Michel C -- AI037526/AI/NIAID NIH HHS/ -- GM007739/GM/NIGMS NIH HHS/ -- GM103314/GM/NIGMS NIH HHS/ -- R01 AI037526/AI/NIAID NIH HHS/ -- RR00862/RR/NCRR NIH HHS/ -- RR022220/RR/NCRR NIH HHS/ -- Howard Hughes Medical Institute/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Feb 8;339(6120):711-5. doi: 10.1126/science.1230624. Epub 2013 Jan 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory of Molecular Immunology, The Rockefeller University, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23306439" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Ataxia Telangiectasia Mutated Proteins ; B-Lymphocytes/immunology/metabolism ; Cell Cycle Proteins/antagonists & inhibitors/metabolism ; Cells, Cultured ; Chromosomal Proteins, Non-Histone/*metabolism ; DNA/*metabolism ; *DNA Breaks, Double-Stranded ; DNA Repair ; DNA-Binding Proteins/antagonists & inhibitors/*metabolism ; G1 Phase ; G2 Phase ; Genomic Instability ; *Immunoglobulin Class Switching ; Mice ; Phosphorylation ; Protein-Serine-Threonine Kinases/antagonists & inhibitors/metabolism ; S Phase ; Telomere-Binding Proteins/*metabolism ; Tumor Suppressor Proteins/antagonists & inhibitors/metabolism
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    Neuroscience. Neural stem cells, excited (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-03-30
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hsieh, Jenny -- Schneider, Jay W -- New York, N.Y. -- Science. 2013 Mar 29;339(6127):1534-5. doi: 10.1126/science.1237576.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA. jenny.hsieh@utsouthwestern.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23539589" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Brain/*cytology/*physiology ; Calcium Channels/physiology ; Cells, Cultured ; Humans ; Neural Stem Cells/*physiology ; *Neurogenesis ; Receptors, N-Methyl-D-Aspartate/physiology ; *Synaptic Transmission ; gamma-Aminobutyric Acid/physiology
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    Evidence for a common mechanism of SIRT1 regulation by allosteric activators (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-03-09
    Description: A molecule that treats multiple age-related diseases would have a major impact on global health and economics. The SIRT1 deacetylase has drawn attention in this regard as a target for drug design. Yet controversy exists around the mechanism of sirtuin-activating compounds (STACs). We found that specific hydrophobic motifs found in SIRT1 substrates such as PGC-1alpha and FOXO3a facilitate SIRT1 activation by STACs. A single amino acid in SIRT1, Glu(230), located in a structured N-terminal domain, was critical for activation by all previously reported STAC scaffolds and a new class of chemically distinct activators. In primary cells reconstituted with activation-defective SIRT1, the metabolic effects of STACs were blocked. Thus, SIRT1 can be directly activated through an allosteric mechanism common to chemically diverse STACs.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799917/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3799917/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hubbard, Basil P -- Gomes, Ana P -- Dai, Han -- Li, Jun -- Case, April W -- Considine, Thomas -- Riera, Thomas V -- Lee, Jessica E -- E, Sook Yen -- Lamming, Dudley W -- Pentelute, Bradley L -- Schuman, Eli R -- Stevens, Linda A -- Ling, Alvin J Y -- Armour, Sean M -- Michan, Shaday -- Zhao, Huizhen -- Jiang, Yong -- Sweitzer, Sharon M -- Blum, Charles A -- Disch, Jeremy S -- Ng, Pui Yee -- Howitz, Konrad T -- Rolo, Anabela P -- Hamuro, Yoshitomo -- Moss, Joel -- Perni, Robert B -- Ellis, James L -- Vlasuk, George P -- Sinclair, David A -- P01 AG027916/AG/NIA NIH HHS/ -- R01 AG019719/AG/NIA NIH HHS/ -- R01 AG028730/AG/NIA NIH HHS/ -- R37 AG028730/AG/NIA NIH HHS/ -- ZIA HL000659-20/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2013 Mar 8;339(6124):1216-9. doi: 10.1126/science.1231097.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Harvard Medical School, Boston, MA 02115, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23471411" target="_blank"〉PubMed〈/a〉
    Keywords: Allosteric Regulation ; Amino Acid Motifs ; Amino Acid Sequence ; Amino Acid Substitution ; Animals ; Cells, Cultured ; Enzyme Activation ; Forkhead Transcription Factors/chemistry/genetics ; Glutamic Acid/chemistry/genetics ; Heterocyclic Compounds with 4 or More Rings/chemistry/pharmacology ; Humans ; Hydrophobic and Hydrophilic Interactions ; Mice ; Molecular Sequence Data ; Myoblasts/drug effects/enzymology ; Protein Structure, Tertiary ; Sirtuin 1/*chemistry/genetics/*metabolism ; Stilbenes/chemistry/*pharmacology ; Substrate Specificity
    Print ISSN: 0036-8075
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    Staphylococcus aureus degrades neutrophil extracellular traps to promote immune cell death (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-11-16
    Description: Bacterial invasion of host tissues triggers polymorphonuclear leukocytes to release DNA [neutrophil extracellular traps (NETs)], thereby immobilizing microbes for subsequent clearance by innate defenses including macrophage phagocytosis. We report here that Staphylococcus aureus escapes these defenses by converting NETs to deoxyadenosine, which triggers the caspase-3-mediated death of immune cells. Conversion of NETs to deoxyadenosine requires two enzymes, nuclease and adenosine synthase, that are secreted by S. aureus and are necessary for the exclusion of macrophages from staphylococcal abscesses. Thus, the pathogenesis of S. aureus infections has evolved to anticipate host defenses and to repurpose them for the destruction of the immune system.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026193/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4026193/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thammavongsa, Vilasack -- Missiakas, Dominique M -- Schneewind, Olaf -- AI038897/AI/NIAID NIH HHS/ -- AI052474/AI/NIAID NIH HHS/ -- AI057153/AI/NIAID NIH HHS/ -- R01 AI038897/AI/NIAID NIH HHS/ -- R01 AI052474/AI/NIAID NIH HHS/ -- T32 AI007090/AI/NIAID NIH HHS/ -- U54 AI057153/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Nov 15;342(6160):863-6. doi: 10.1126/science.1242255.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Chicago, 920 East 58th Street, Chicago, IL 60637, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24233725" target="_blank"〉PubMed〈/a〉
    Keywords: Abscess/immunology/microbiology ; Animals ; Apoptosis/*immunology ; Cells, Cultured ; Cytotoxicity, Immunologic ; Deoxyadenosines/*metabolism ; Deoxyribonucleases/metabolism ; Host-Pathogen Interactions/*immunology ; Humans ; Macrophages/immunology/microbiology ; Mice, Inbred BALB C ; Neutrophils/*immunology/*microbiology ; Staphylococcal Infections/*immunology ; Staphylococcus aureus/enzymology/*pathogenicity
    Print ISSN: 0036-8075
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    Positive feedback between PU.1 and the cell cycle controls myeloid differentiation (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-07-23
    Description: Regulatory gene circuits with positive-feedback loops control stem cell differentiation, but several mechanisms can contribute to positive feedback. Here, we dissect feedback mechanisms through which the transcription factor PU.1 controls lymphoid and myeloid differentiation. Quantitative live-cell imaging revealed that developing B cells decrease PU.1 levels by reducing PU.1 transcription, whereas developing macrophages increase PU.1 levels by lengthening their cell cycles, which causes stable PU.1 accumulation. Exogenous PU.1 expression in progenitors increases endogenous PU.1 levels by inducing cell cycle lengthening, implying positive feedback between a regulatory factor and the cell cycle. Mathematical modeling showed that this cell cycle-coupled feedback architecture effectively stabilizes a slow-dividing differentiated state. These results show that cell cycle duration functions as an integral part of a positive autoregulatory circuit to control cell fate.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3913367/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3913367/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kueh, Hao Yuan -- Champhekar, Ameya -- Nutt, Stephen L -- Elowitz, Michael B -- Rothenberg, Ellen V -- R01 AI083514/AI/NIAID NIH HHS/ -- R01 CA090233/CA/NCI NIH HHS/ -- R01 CA90233/CA/NCI NIH HHS/ -- R33 HL089123/HL/NHLBI NIH HHS/ -- RC2 CA148278/CA/NCI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Aug 9;341(6146):670-3. doi: 10.1126/science.1240831. Epub 2013 Jul 18.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Biology, California Institute of Technology, Pasadena, CA, USA. kueh@caltech.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23868921" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Cycle/*genetics ; Cell Differentiation/*genetics ; Cells, Cultured ; Feedback, Physiological ; *Gene Expression Regulation ; *Gene Regulatory Networks ; Macrophages/cytology ; Mice ; Mice, Inbred Strains ; Myeloid Cells/*cytology ; Precursor Cells, B-Lymphoid/*cytology ; Proto-Oncogene Proteins/genetics/*physiology ; Trans-Activators/genetics/*physiology
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    Mucus enhances gut homeostasis and oral tolerance by delivering immunoregulatory signals (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-09-28
    Description: A dense mucus layer in the large intestine prevents inflammation by shielding the underlying epithelium from luminal bacteria and food antigens. This mucus barrier is organized around the hyperglycosylated mucin MUC2. Here we show that the small intestine has a porous mucus layer, which permitted the uptake of MUC2 by antigen-sampling dendritic cells (DCs). Glycans associated with MUC2 imprinted DCs with anti-inflammatory properties by assembling a galectin-3-Dectin-1-FcgammaRIIB receptor complex that activated beta-catenin. This transcription factor interfered with DC expression of inflammatory but not tolerogenic cytokines by inhibiting gene transcription through nuclear factor kappaB. MUC2 induced additional conditioning signals in intestinal epithelial cells. Thus, mucus does not merely form a nonspecific physical barrier, but also constrains the immunogenicity of gut antigens by delivering tolerogenic signals.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005805/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4005805/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Shan, Meimei -- Gentile, Maurizio -- Yeiser, John R -- Walland, A Cooper -- Bornstein, Victor U -- Chen, Kang -- He, Bing -- Cassis, Linda -- Bigas, Anna -- Cols, Montserrat -- Comerma, Laura -- Huang, Bihui -- Blander, J Magarian -- Xiong, Huabao -- Mayer, Lloyd -- Berin, Cecilia -- Augenlicht, Leonard H -- Velcich, Anna -- Cerutti, Andrea -- AI073899/AI/NIAID NIH HHS/ -- AI095245/AI/NIAID NIH HHS/ -- AI57653/AI/NIAID NIH HHS/ -- AI61093/AI/NIAID NIH HHS/ -- AI74378/AI/NIAID NIH HHS/ -- AI95613/AI/NIAID NIH HHS/ -- AI96187/AI/NIAID NIH HHS/ -- DK072201/DK/NIDDK NIH HHS/ -- P01 AI061093/AI/NIAID NIH HHS/ -- P01 DK072201/DK/NIDDK NIH HHS/ -- P60 DK020541/DK/NIDDK NIH HHS/ -- R01 AI057653/AI/NIAID NIH HHS/ -- R01 AI093577/AI/NIAID NIH HHS/ -- U01 AI095613/AI/NIAID NIH HHS/ -- U19 AI096187/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2013 Oct 25;342(6157):447-53. doi: 10.1126/science.1237910. Epub 2013 Sep 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, Immunology Institute, Icahn School of Medicine at Mount Sinai, New York, NY, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24072822" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Dendritic Cells/immunology ; Galectin 3/genetics/metabolism ; Glycosylation ; *Homeostasis ; Humans ; Immune Tolerance/genetics/*immunology ; Inflammation/immunology ; Intestinal Mucosa/immunology ; Intestine, Small/*immunology ; Lectins, C-Type/genetics/metabolism ; Mice ; Mice, Inbred C57BL ; Mice, Mutant Strains ; Mouth/*immunology ; Mucin-2/genetics/physiology ; Mucus/*immunology ; NF-kappa B/metabolism ; Receptors, IgG/genetics/metabolism ; Transcription, Genetic ; beta Catenin/metabolism
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    BTBD3 controls dendrite orientation toward active axons in mammalian neocortex (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-11-02
    Description: Experience-dependent structural changes in the developing brain are fundamental for proper neural circuit formation. Here, we show that during the development of the sensory cortex, dendritic field orientation is controlled by the BTB/POZ domain-containing 3 (BTBD3). In developing mouse somatosensory cortex, endogenous Btbd3 translocated to the cell nucleus in response to neuronal activity and oriented primary dendrites toward active axons in the barrel hollow. Btbd3 also directed dendrites toward active axon terminals when ectopically expressed in mouse visual cortex or normally expressed in ferret visual cortex. BTBD3 regulation of dendrite orientation is conserved across species and cortical areas and shows how high-acuity sensory function may be achieved by the tuning of subcellular polarity to sources of high sensory activity.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Matsui, Asuka -- Tran, May -- Yoshida, Aya C -- Kikuchi, Satomi S -- U, Mami -- Ogawa, Masaharu -- Shimogori, Tomomi -- New York, N.Y. -- Science. 2013 Nov 29;342(6162):1114-8. doi: 10.1126/science.1244505. Epub 2013 Oct 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉RIKEN Brain Science Institute, Laboratory for Molecular Mechanisms of Thalamus Development, 2-1 Hirosawa Wako, Saitama 351-0198, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24179155" target="_blank"〉PubMed〈/a〉
    Keywords: Active Transport, Cell Nucleus ; Animals ; Axons/*physiology ; Cell Nucleus/metabolism ; *Cell Polarity ; Cells, Cultured ; Dendrites/*physiology ; Ferrets ; Gene Knockdown Techniques ; Mice ; Mice, Mutant Strains ; Neocortex/*embryology ; Nerve Net/*growth & development ; Nerve Tissue Proteins/genetics/*metabolism ; Visual Cortex/*embryology
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    A localized Wnt signal orients asymmetric stem cell division in vitro (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-03-23
    Description: Developmental signals such as Wnts are often presented to cells in an oriented manner. To examine the consequences of local Wnt signaling, we immobilized Wnt proteins on beads and introduced them to embryonic stem cells in culture. At the single-cell level, the Wnt-bead induced asymmetric distribution of Wnt-beta-catenin signaling components, oriented the plane of mitotic division, and directed asymmetric inheritance of centrosomes. Before cytokinesis was completed, the Wnt-proximal daughter cell expressed high levels of nuclear beta-catenin and pluripotency genes, whereas the distal daughter cell acquired hallmarks of differentiation. We suggest that a spatially restricted Wnt signal induces an oriented cell division that generates distinct cell fates at predictable positions relative to the Wnt source.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966430/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3966430/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Habib, Shukry J -- Chen, Bi-Chang -- Tsai, Feng-Chiao -- Anastassiadis, Konstantinos -- Meyer, Tobias -- Betzig, Eric -- Nusse, Roel -- 102513/Wellcome Trust/United Kingdom -- GM063702/GM/NIGMS NIH HHS/ -- NS069375/NS/NINDS NIH HHS/ -- R01 GM030179/GM/NIGMS NIH HHS/ -- R01 GM063702/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Mar 22;339(6126):1445-8. doi: 10.1126/science.1231077.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Developmental Biology, Howard Hughes Medical Institute, Institute for Stem Cell Biology and Regenerative Medicine, Stanford University, 265 Campus Drive, Stanford, CA 94305, USA. shabib@stanford.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23520113" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Asymmetric Cell Division ; *Cell Differentiation ; Cells, Cultured ; Centrosome/physiology ; Cytokinesis ; Embryonic Stem Cells/*cytology/*metabolism ; Gene Expression ; Homeodomain Proteins/genetics/metabolism ; Mice ; Mitosis ; Octamer Transcription Factor-3/genetics/metabolism ; Pluripotent Stem Cells/physiology ; Recombinant Proteins/metabolism ; Single-Cell Analysis ; Transcription Factors/genetics/metabolism ; Wnt Proteins/metabolism ; *Wnt Signaling Pathway ; Wnt3A Protein/*metabolism ; beta Catenin/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Yeast reveal a "druggable" Rsp5/Nedd4 network that ameliorates alpha-synuclein toxicity in neurons (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-10-26
    Description: alpha-Synuclein (alpha-syn) is a small lipid-binding protein implicated in several neurodegenerative diseases, including Parkinson's disease, whose pathobiology is conserved from yeast to man. There are no therapies targeting these underlying cellular pathologies, or indeed those of any major neurodegenerative disease. Using unbiased phenotypic screens as an alternative to target-based approaches, we discovered an N-aryl benzimidazole (NAB) that strongly and selectively protected diverse cell types from alpha-syn toxicity. Three chemical genetic screens in wild-type yeast cells established that NAB promoted endosomal transport events dependent on the E3 ubiquitin ligase Rsp5/Nedd4. These same steps were perturbed by alpha-syn itself. Thus, NAB identifies a druggable node in the biology of alpha-syn that can correct multiple aspects of its underlying pathology, including dysfunctional endosomal and endoplasmic reticulum-to-Golgi vesicle trafficking.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993916/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3993916/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Tardiff, Daniel F -- Jui, Nathan T -- Khurana, Vikram -- Tambe, Mitali A -- Thompson, Michelle L -- Chung, Chee Yeun -- Kamadurai, Hari B -- Kim, Hyoung Tae -- Lancaster, Alex K -- Caldwell, Kim A -- Caldwell, Guy A -- Rochet, Jean-Christophe -- Buchwald, Stephen L -- Lindquist, Susan -- 5R01GM069530/GM/NIGMS NIH HHS/ -- F32GM099817/GM/NIGMS NIH HHS/ -- F32NS061419/NS/NINDS NIH HHS/ -- GM58160/GM/NIGMS NIH HHS/ -- K01 AG038546/AG/NIA NIH HHS/ -- R01 GM058160/GM/NIGMS NIH HHS/ -- R15 NS075684/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 22;342(6161):979-83. doi: 10.1126/science.1245321. Epub 2013 Oct 24.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Whitehead Institute for Biomedical Research (WIBR), Cambridge, MA 02142, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24158909" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Benzimidazoles/chemistry/*pharmacology ; Caenorhabditis elegans ; Cells, Cultured ; *Cytoprotection ; Drug Evaluation, Preclinical ; Endosomal Sorting Complexes Required for Transport/*genetics ; Gene Regulatory Networks/*drug effects ; Neurodegenerative Diseases/*metabolism ; Neurons/*drug effects/metabolism ; Neuroprotective Agents/*pharmacology ; Parkinson Disease/metabolism ; Rats ; Saccharomyces cerevisiae/drug effects ; Saccharomyces cerevisiae Proteins/*genetics ; Small Molecule Libraries/chemistry/pharmacology ; Ubiquitin-Protein Ligase Complexes/*genetics ; Ubiquitin-Protein Ligases/*genetics ; alpha-Synuclein/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Supercomplex assembly determines electron flux in the mitochondrial electron transport chain (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-07-03
    Description: The textbook description of mitochondrial respiratory complexes (RCs) views them as free-moving entities linked by the mobile carriers coenzyme Q (CoQ) and cytochrome c (cyt c). This model (known as the fluid model) is challenged by the proposal that all RCs except complex II can associate in supercomplexes (SCs). The proposed SCs are the respirasome (complexes I, III, and IV), complexes I and III, and complexes III and IV. The role of SCs is unclear, and their existence is debated. By genetic modulation of interactions between complexes I and III and III and IV, we show that these associations define dedicated CoQ and cyt c pools and that SC assembly is dynamic and organizes electron flux to optimize the use of available substrates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lapuente-Brun, Esther -- Moreno-Loshuertos, Raquel -- Acin-Perez, Rebeca -- Latorre-Pellicer, Ana -- Colas, Carmen -- Balsa, Eduardo -- Perales-Clemente, Ester -- Quiros, Pedro M -- Calvo, Enrique -- Rodriguez-Hernandez, M A -- Navas, Placido -- Cruz, Raquel -- Carracedo, Angel -- Lopez-Otin, Carlos -- Perez-Martos, Acisclo -- Fernandez-Silva, Patricio -- Fernandez-Vizarra, Erika -- Enriquez, Jose Antonio -- New York, N.Y. -- Science. 2013 Jun 28;340(6140):1567-70. doi: 10.1126/science.1230381.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Centro Nacional de Investigaciones Cardiovasculares Carlos III, Madrid, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23812712" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cells, Cultured ; Cytochromes c/*metabolism ; Electron Transport ; Electron Transport Complex I/genetics/*metabolism ; Electron Transport Complex III/genetics/*metabolism ; Electron Transport Complex IV/genetics/*metabolism ; Gene Knockdown Techniques ; HEK293 Cells ; Humans ; Mice ; Mice, Inbred C57BL ; Mitochondria/*enzymology ; Molecular Sequence Data ; Ubiquinone/*metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Long-distance integration of nuclear ERK signaling triggered by activation of a few dendritic spines (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-11-30
    Description: The late phase of long-term potentiation (LTP) at glutamatergic synapses, which is thought to underlie long-lasting memory, requires gene transcription in the nucleus. However, the mechanism by which signaling initiated at synapses is transmitted into the nucleus to induce transcription has remained elusive. Here, we found that induction of LTP in only three to seven dendritic spines in rat CA1 pyramidal neurons was sufficient to activate extracellular signal-regulated kinase (ERK) in the nucleus and regulate downstream transcription factors. Signaling from individual spines was integrated over a wide range of time (〉30 minutes) and space (〉80 micrometers). Spatially dispersed inputs over multiple branches activated nuclear ERK much more efficiently than clustered inputs over one branch. Thus, biochemical signals from individual dendritic spines exert profound effects on nuclear signaling.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4318497/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4318497/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Zhai, Shenyu -- Ark, Eugene D -- Parra-Bueno, Paula -- Yasuda, Ryohei -- R01 MH080047/MH/NIMH NIH HHS/ -- R01 NS068410/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2013 Nov 29;342(6162):1107-11. doi: 10.1126/science.1245622.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Duke University Medical Center, Durham, NC 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24288335" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CA1 Region, Hippocampal/enzymology/*physiology ; Cells, Cultured ; Dendritic Spines/enzymology/*physiology ; Extracellular Signal-Regulated MAP Kinases/*metabolism ; Glutamates/metabolism ; *Long-Term Potentiation ; Rats ; Signal Transduction ; Transcription Factors/metabolism
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Hedgehog signaling controls T cell killing at the immunological synapse (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-07
    Description: The centrosome is essential for cytotoxic T lymphocyte (CTL) function, contacting the plasma membrane and directing cytotoxic granules for secretion at the immunological synapse. Centrosome docking at the plasma membrane also occurs during cilia formation. The primary cilium, formed in nonhematopoietic cells, is essential for vertebrate Hedgehog (Hh) signaling. Lymphocytes do not form primary cilia, but we found and describe here that Hh signaling played an important role in CTL killing. T cell receptor activation, which "prearms" CTLs with cytotoxic granules, also initiated Hh signaling. Hh pathway activation occurred intracellularly and triggered Rac1 synthesis. These events "prearmed" CTLs for action by promoting the actin remodeling required for centrosome polarization and granule release. Thus, Hh signaling plays a role in CTL function, and the immunological synapse may represent a modified cilium.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022134/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4022134/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉de la Roche, Maike -- Ritter, Alex T -- Angus, Karen L -- Dinsmore, Colin -- Earnshaw, Charles H -- Reiter, Jeremy F -- Griffiths, Gillian M -- 075880/Wellcome Trust/United Kingdom -- 100140/Wellcome Trust/United Kingdom -- R01 AR054396/AR/NIAMS NIH HHS/ -- R01 GM095941/GM/NIGMS NIH HHS/ -- R01AR05439/AR/NIAMS NIH HHS/ -- R01GM095941/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2013 Dec 6;342(6163):1247-50. doi: 10.1126/science.1244689.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cambridge Institute for Medical Research, University of Cambridge, Hills Road, Cambridge CB2 0XY, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24311692" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; CD8-Positive T-Lymphocytes/*immunology/metabolism ; Cell Polarity ; Cells, Cultured ; Centrosome/metabolism ; *Cytotoxicity, Immunologic ; Hedgehog Proteins/*metabolism ; *Immunological Synapses ; Kruppel-Like Transcription Factors/genetics/metabolism ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Immunological ; Neuropeptides/genetics/metabolism ; Receptors, Antigen, T-Cell/immunology/metabolism ; Receptors, Cell Surface/metabolism ; Receptors, G-Protein-Coupled/metabolism ; *Signal Transduction ; T-Lymphocytes, Cytotoxic/*immunology/metabolism ; rac1 GTP-Binding Protein/genetics/metabolism
    Print ISSN: 0036-8075
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    Quantitative phosphoproteomics reveal mTORC1 activates de novo pyrimidine synthesis (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-02-23
    Description: The Ser-Thr kinase mammalian target of rapamycin (mTOR) controls cell growth and metabolism by stimulating glycolysis and synthesis of proteins and lipids. To further understand the central role of mTOR in cell physiology, we used quantitative phosphoproteomics to identify substrates or downstream effectors of the two mTOR complexes. mTOR controlled the phosphorylation of 335 proteins, including CAD (carbamoyl-phosphate synthetase 2, aspartate transcarbamylase, and dihydroorotase). CAD catalyzes the first three steps in de novo pyrimidine synthesis. mTORC1 indirectly phosphorylated CAD-S1859 through S6 kinase (S6K). CAD-S1859 phosphorylation promoted CAD oligomerization and thereby stimulated de novo synthesis of pyrimidines and progression through S phase of the cell cycle in mammalian cells. Thus, mTORC1 also stimulates the synthesis of nucleotides to control cell proliferation.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Robitaille, Aaron M -- Christen, Stefan -- Shimobayashi, Mitsugu -- Cornu, Marion -- Fava, Luca L -- Moes, Suzette -- Prescianotto-Baschong, Cristina -- Sauer, Uwe -- Jenoe, Paul -- Hall, Michael N -- New York, N.Y. -- Science. 2013 Mar 15;339(6125):1320-3. doi: 10.1126/science.1228771. Epub 2013 Feb 21.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Biozentrum, University of Basel, Basel, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23429704" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aspartate Carbamoyltransferase/genetics/*metabolism ; Carbamoyl-Phosphate Synthase (Glutamine-Hydrolyzing)/genetics/*metabolism ; Cells, Cultured ; Dihydroorotase/genetics/*metabolism ; HeLa Cells ; Humans ; Mice ; Mice, Knockout ; Multiprotein Complexes/*metabolism ; Phosphoproteins/*metabolism ; Proteome/metabolism ; Pyrimidines/*biosynthesis ; TOR Serine-Threonine Kinases/*metabolism
    Print ISSN: 0036-8075
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    A secreted disulfide catalyst controls extracellular matrix composition and function (2013)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2013-05-25
    Description: Disulfide bond formation in secretory proteins occurs primarily in the endoplasmic reticulum (ER), where multiple enzyme families catalyze cysteine cross-linking. Quiescin sulfhydryl oxidase 1 (QSOX1) is an atypical disulfide catalyst, localized to the Golgi apparatus or secreted from cells. We examined the physiological function for extracellular catalysis of de novo disulfide bond formation by QSOX1. QSOX1 activity was required for incorporation of laminin into the extracellular matrix (ECM) synthesized by fibroblasts, and ECM produced without QSOX1 was defective in supporting cell-matrix adhesion. We developed an inhibitory monoclonal antibody against QSOX1 that could modulate ECM properties and undermine cell migration.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ilani, Tal -- Alon, Assaf -- Grossman, Iris -- Horowitz, Ben -- Kartvelishvily, Elena -- Cohen, Sidney R -- Fass, Deborah -- New York, N.Y. -- Science. 2013 Jul 5;341(6141):74-6. doi: 10.1126/science.1238279. Epub 2013 May 23.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Structural Biology, Weizmann Institute of Science, Rehovot, Israel. tal.ilani@weizmann.ac.il〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23704371" target="_blank"〉PubMed〈/a〉
    Keywords: Antibodies, Monoclonal ; Cell Adhesion ; Cell Line, Tumor ; Cell Movement ; Cells, Cultured ; Cysteine/metabolism ; Disulfides/metabolism ; Extracellular Matrix/enzymology/*physiology/ultrastructure ; Fibroblasts/enzymology/ultrastructure ; Humans ; Laminin/metabolism ; Oxidoreductases Acting on Sulfur Group Donors/antagonists & ; inhibitors/*metabolism
    Print ISSN: 0036-8075
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    IFI16 DNA sensor is required for death of lymphoid CD4 T cells abortively infected with HIV (2013)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2013-12-21
    Description: The progressive depletion of quiescent "bystander" CD4 T cells, which are nonpermissive to HIV infection, is a principal driver of the acquired immunodeficiency syndrome (AIDS). These cells undergo abortive infection characterized by the cytosolic accumulation of incomplete HIV reverse transcripts. These viral DNAs are sensed by an unidentified host sensor that triggers an innate immune response, leading to caspase-1 activation and pyroptosis. Using unbiased proteomic and targeted biochemical approaches, as well as two independent methods of lentiviral short hairpin RNA-mediated gene knockdown in primary CD4 T cells, we identify interferon-gamma-inducible protein 16 (IFI16) as a host DNA sensor required for CD4 T cell death due to abortive HIV infection. These findings provide insights into a key host pathway that plays a central role in CD4 T cell depletion during disease progression to AIDS.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3976200/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3976200/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Monroe, Kathryn M -- Yang, Zhiyuan -- Johnson, Jeffrey R -- Geng, Xin -- Doitsh, Gilad -- Krogan, Nevan J -- Greene, Warner C -- 1DP1036502/DP/NCCDPHP CDC HHS/ -- DP1 DA036502/DA/NIDA NIH HHS/ -- P01 AI090935/AI/NIAID NIH HHS/ -- P30 AI027763/AI/NIAID NIH HHS/ -- P50 GM081879/GM/NIGMS NIH HHS/ -- P50 GM082250/GM/NIGMS NIH HHS/ -- R21 AI102782/AI/NIAID NIH HHS/ -- U19 AI096113/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2014 Jan 24;343(6169):428-32. doi: 10.1126/science.1243640. Epub 2013 Dec 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Gladstone Institute of Virology and Immunology, 1650 Owens Street, San Francisco, CA 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24356113" target="_blank"〉PubMed〈/a〉
    Keywords: Acquired Immunodeficiency Syndrome/*immunology ; Apoptosis/*immunology ; CD4-Positive T-Lymphocytes/*immunology/*virology ; Cells, Cultured ; DNA, Viral/*immunology ; DNA-Binding Proteins/genetics/immunology ; Gene Knockdown Techniques ; HEK293 Cells ; HIV-1/*immunology ; Humans ; Immunity, Innate ; Lymphocyte Depletion ; Nuclear Proteins/genetics/*immunology ; Palatine Tonsil/immunology ; Phosphoproteins/genetics/*immunology ; RNA, Small Interfering/genetics ; Spleen/immunology
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    Elfn1 regulates target-specific release probability at CA1-interneuron synapses (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-09
    Description: Although synaptic transmission may be unidirectional, the establishment of synaptic connections with specific properties can involve bidirectional signaling. Pyramidal neurons in the hippocampus form functionally distinct synapses onto two types of interneurons. Excitatory synapses onto oriens-lacunosum moleculare (O-LM) interneurons are facilitating and have a low release probability, whereas synapses onto parvalbumin interneurons are depressing and have a high release probability. Here, we show that the extracellular leucine-rich repeat fibronectin containing 1 (Elfn1) protein is selectively expressed by O-LM interneurons and regulates presynaptic release probability to direct the formation of highly facilitating pyramidal-O-LM synapses. Thus, postsynaptic expression of Elfn1 in O-LM interneurons regulates presynaptic release probability, which confers target-specific synaptic properties to pyramidal cell axons.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sylwestrak, Emily L -- Ghosh, Anirvan -- R01 NS067216/NS/NINDS NIH HHS/ -- R01NS067216/NS/NINDS NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 26;338(6106):536-40. doi: 10.1126/science.1222482. Epub 2012 Oct 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Neurobiology Section, Division of Biological Sciences, University of California, San Diego, La Jolla, CA 92093-0366, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23042292" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Axons/metabolism ; CA1 Region, Hippocampal/*metabolism ; Cells, Cultured ; Gene Knockdown Techniques ; Green Fluorescent Proteins/genetics/metabolism ; HEK293 Cells ; Humans ; Interneurons/*metabolism ; Mice ; Nerve Tissue Proteins/genetics/*metabolism ; RNA, Small Interfering/metabolism ; Rats ; Rats, Inbred LEC ; Synapses/genetics/*metabolism ; Synaptic Transmission
    Print ISSN: 0036-8075
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A single progenitor population switches behavior to maintain and repair esophageal epithelium (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-07-24
    Description: Diseases of the esophageal epithelium (EE), such as reflux esophagitis and cancer, are rising in incidence. Despite this, the cellular behaviors underlying EE homeostasis and repair remain controversial. Here, we show that in mice, EE is maintained by a single population of cells that divide stochastically to generate proliferating and differentiating daughters with equal probability. In response to challenge with all-trans retinoic acid (atRA), the balance of daughter cell fate is unaltered, but the rate of cell division increases. However, after wounding, cells reversibly switch to producing an excess of proliferating daughters until the wound has closed. Such fate-switching enables a single progenitor population to both maintain and repair tissue without the need for a "reserve" slow-cycling stem cell pool.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527005/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3527005/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Doupe, David P -- Alcolea, Maria P -- Roshan, Amit -- Zhang, Gen -- Klein, Allon M -- Simons, Benjamin D -- Jones, Philip H -- 079249/Wellcome Trust/United Kingdom -- 092096/Wellcome Trust/United Kingdom -- G0601740/Medical Research Council/United Kingdom -- G0700600/1/National Centre for the Replacement, Refinement and Reduction of Animals in Research/United Kingdom -- G0800784/Medical Research Council/United Kingdom -- MC_U105370181/Medical Research Council/United Kingdom -- U.1053.00.010(70181)/Medical Research Council/United Kingdom -- Medical Research Council/United Kingdom -- Wellcome Trust/United Kingdom -- New York, N.Y. -- Science. 2012 Aug 31;337(6098):1091-3. doi: 10.1126/science.1218835. Epub 2012 Jul 19.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Medical Research Council (MRC) Cancer Cell Unit, Hutchison-MRC Research Centre, Cambridge, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22821983" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Biomarkers/analysis ; Cell Differentiation/drug effects ; Cell Division/drug effects ; Cell Proliferation/drug effects ; Cells, Cultured ; Doxycycline/pharmacology ; Epithelial Cells/*physiology ; Epithelium/drug effects/metabolism/*physiology ; Esophagus/*cytology/*physiology ; Green Fluorescent Proteins/biosynthesis ; Histones/biosynthesis ; Mice ; Mice, Inbred C57BL ; Recombinant Fusion Proteins/biosynthesis ; *Regeneration ; Stem Cells/metabolism/*physiology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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    A periciliary brush promotes the lung health by separating the mucus layer from airway epithelia (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-08-28
    Description: Mucus clearance is the primary defense mechanism that protects airways from inhaled infectious and toxic agents. In the current gel-on-liquid mucus clearance model, a mucus gel is propelled on top of a "watery" periciliary layer surrounding the cilia. However, this model fails to explain the formation of a distinct mucus layer in health or why mucus clearance fails in disease. We propose a gel-on-brush model in which the periciliary layer is occupied by membrane-spanning mucins and mucopolysaccharides densely tethered to the airway surface. This brush prevents mucus penetration into the periciliary space and causes mucus to form a distinct layer. The relative osmotic moduli of the mucus and periciliary brush layers explain both the stability of mucus clearance in health and its failure in airway disease.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3633213/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3633213/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Button, Brian -- Cai, Li-Heng -- Ehre, Camille -- Kesimer, Mehmet -- Hill, David B -- Sheehan, John K -- Boucher, Richard C -- Rubinstein, Michael -- HHSN268200900020/PHS HHS/ -- K01DK080847/DK/NIDDK NIH HHS/ -- P01HL108808/HL/NHLBI NIH HHS/ -- P01HL110873-01/HL/NHLBI NIH HHS/ -- P01HL34322/HL/NHLBI NIH HHS/ -- P30DK065988/DK/NIDDK NIH HHS/ -- P50HL107168/HL/NHLBI NIH HHS/ -- P50HL107168-01/HL/NHLBI NIH HHS/ -- R01 HL103940/HL/NHLBI NIH HHS/ -- R01HL077546/HL/NHLBI NIH HHS/ -- R01HL103940/HL/NHLBI NIH HHS/ -- UL1-RR025747/RR/NCRR NIH HHS/ -- New York, N.Y. -- Science. 2012 Aug 24;337(6097):937-41. doi: 10.1126/science.1223012.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Cystic Fibrosis Research and Treatment Center, University of North Carolina, Chapel Hill, NC 27599-7248, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22923574" target="_blank"〉PubMed〈/a〉
    Keywords: Cells, Cultured ; Cilia/*physiology/ultrastructure ; Gels ; Glycosaminoglycans/*physiology ; Humans ; Lung/*physiology ; Lung Diseases/physiopathology ; *Models, Biological ; Mucins/*physiology ; *Mucociliary Clearance ; Mucus/*physiology ; Osmotic Pressure ; Respiratory Mucosa/*physiology/ultrastructure
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    Profile: Kit Parker. Engineering a new line of attack on a signature war injury (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-10
    Description: 〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miller, Greg -- New York, N.Y. -- Science. 2012 Jan 6;335(6064):33-5. doi: 10.1126/science.335.6064.33.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22223790" target="_blank"〉PubMed〈/a〉
    Keywords: Afghan Campaign 2001- ; Animals ; Axons/pathology ; Blast Injuries/pathology/*physiopathology ; Brain Injuries/epidemiology/pathology/*physiopathology ; Cells, Cultured ; History, 21st Century ; Humans ; Integrins/metabolism ; Iraq War, 2003-2011 ; Neurons/physiology ; Tissue Engineering ; Vasospasm, Intracranial/pathology/physiopathology
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    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 94
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    Airn transcriptional overlap, but not its lncRNA products, induces imprinted Igf2r silencing (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-12-15
    Description: Mammalian imprinted genes often cluster with long noncoding (lnc) RNAs. Three lncRNAs that induce parental-specific silencing show hallmarks indicating that their transcription is more important than their product. To test whether Airn transcription or product silences the Igf2r gene, we shortened the endogenous lncRNA to different lengths. The results excluded a role for spliced and unspliced Airn lncRNA products and for Airn nuclear size and location in silencing Igf2r. Instead, silencing only required Airn transcriptional overlap of the Igf2r promoter, which interferes with RNA polymerase II recruitment in the absence of repressive chromatin. Such a repressor function for lncRNA transcriptional overlap reveals a gene silencing mechanism that may be widespread in the mammalian genome, given the abundance of lncRNA transcripts.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Latos, Paulina A -- Pauler, Florian M -- Koerner, Martha V -- Senergin, H Basak -- Hudson, Quanah J -- Stocsits, Roman R -- Allhoff, Wolfgang -- Stricker, Stefan H -- Klement, Ruth M -- Warczok, Katarzyna E -- Aumayr, Karin -- Pasierbek, Pawel -- Barlow, Denise P -- New York, N.Y. -- Science. 2012 Dec 14;338(6113):1469-72. doi: 10.1126/science.1228110.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, Lazarettgasse 14, 1090 Vienna, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23239737" target="_blank"〉PubMed〈/a〉
    Keywords: Alternative Splicing ; Animals ; Cells, Cultured ; *Gene Silencing ; *Genomic Imprinting ; Mice ; Multigene Family ; Promoter Regions, Genetic ; RNA Polymerase II/metabolism ; RNA, Long Noncoding/genetics/*metabolism ; Receptor, IGF Type 2/*genetics ; *Transcription, Genetic
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  • 95
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    Asymmetric segregation of polarized antigen on B cell division shapes presentation capacity (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-01-28
    Description: During the activation of humoral immune responses, B cells acquire antigen for subsequent presentation to cognate T cells. Here we show that after mouse B cells accumulate antigen, it is maintained in a polarized distribution for extended periods in vivo. Using high-throughput imaging flow cytometry, we observed that this polarization is preserved during B cell division, promoting asymmetric antigen segregation among progeny. Antigen inheritance correlates with the ability of progeny to activate T cells: Daughter cells receiving larger antigen stores exhibit a prolonged capacity to present antigen, which renders them more effective in competing for T cell help. The generation of progeny with differential capacities for antigen presentation may have implications for somatic hypermutation and class switching during affinity maturation and as B cells commit to effector cell fates.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Thaunat, Olivier -- Granja, Aitor G -- Barral, Patricia -- Filby, Andrew -- Montaner, Beatriz -- Collinson, Lucy -- Martinez-Martin, Nuria -- Harwood, Naomi E -- Bruckbauer, Andreas -- Batista, Facundo D -- Cancer Research UK/United Kingdom -- New York, N.Y. -- Science. 2012 Jan 27;335(6067):475-9. doi: 10.1126/science.1214100.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Lymphocyte Interaction Laboratory, London Research Institute, Cancer Research UK, 44 Lincoln's Inn Fields, London, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22282815" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Antigen Presentation ; Antigens/*analysis/*immunology ; B-Lymphocytes/cytology/*immunology ; Cell Division ; Cell Proliferation ; Cells, Cultured ; Coculture Techniques ; Computer Simulation ; Flow Cytometry ; *Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Mice, Transgenic ; Models, Immunological ; Muramidase/analysis/immunology ; T-Lymphocytes/*immunology
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  • 96
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    Wnt5a potentiates TGF-beta signaling to promote colonic crypt regeneration after tissue injury (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-09-08
    Description: Reestablishing homeostasis after tissue damage depends on the proper organization of stem cells and their progeny, though the repair mechanisms are unclear. The mammalian intestinal epithelium is well suited to approach this problem, as it is composed of well-delineated units called crypts of Lieberkuhn. We found that Wnt5a, a noncanonical Wnt ligand, was required for crypt regeneration after injury in mice. Unlike controls, Wnt5a-deficient mice maintained an expanded population of proliferative epithelial cells in the wound. We used an in vitro system to enrich for intestinal epithelial stem cells to discover that Wnt5a inhibited proliferation of these cells. Surprisingly, the effects of Wnt5a were mediated by activation of transforming growth factor-beta (TGF-beta) signaling. These findings suggest a Wnt5a-dependent mechanism for forming new crypt units to reestablish homeostasis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3706630/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3706630/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Miyoshi, Hiroyuki -- Ajima, Rieko -- Luo, Christine T -- Yamaguchi, Terry P -- Stappenbeck, Thaddeus S -- 5T35DK074375/DK/NIDDK NIH HHS/ -- DK90251/DK/NIDDK NIH HHS/ -- P30-DK52574/DK/NIDDK NIH HHS/ -- R01 DK071619/DK/NIDDK NIH HHS/ -- Intramural NIH HHS/ -- New York, N.Y. -- Science. 2012 Oct 5;338(6103):108-13. doi: 10.1126/science.1223821. Epub 2012 Sep 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, MO 63110, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22956684" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Movement/drug effects/physiology ; Cell Proliferation/drug effects ; Cells, Cultured ; Colon/embryology/*injuries/*physiology ; Culture Media, Conditioned/pharmacology ; Homeostasis/drug effects/physiology ; Intestinal Mucosa/embryology/injuries/physiology ; Ligands ; Mesoderm/cytology/embryology ; Mice ; Mice, Knockout ; Receptor Tyrosine Kinase-like Orphan Receptors/metabolism ; Recombinant Proteins/pharmacology ; Signal Transduction ; Stem Cells/cytology/drug effects/physiology ; Tamoxifen/pharmacology ; Transforming Growth Factor beta/*metabolism ; Wnt Proteins/genetics/pharmacology/*physiology ; Wound Healing/drug effects/*physiology
    Print ISSN: 0036-8075
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    Pigment pattern formation by contact-dependent depolarization (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-02-11
    Description: Although recent experimental studies have suggested that the interactions among the pigment cells play a key role in the skin pattern formation, details of the mechanism remain largely unknown. By using an in vitro cell culture system, we have detected interactions between the two pigment cell types, melanophores and xanthophores, in the zebrafish skin. During primary culture, the melanophore membrane transiently depolarizes when contacted with the dendrites of a xanthophore. This depolarization triggers melanophore migration to avoid further contact with the xanthophores. Cell depolarization and repulsive movement were not observed in pigment cells with the jaguar mutant, which shows defective segregation of melanophores and xanthophores. The depolarization-repulsion of wild-type pigment cells may explain the pigment cell behaviors generating the stripe pattern of zebrafish.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Inaba, Masafumi -- Yamanaka, Hiroaki -- Kondo, Shigeru -- New York, N.Y. -- Science. 2012 Feb 10;335(6069):677. doi: 10.1126/science.1212821.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Graduate School of Frontier Biosciences, Osaka University, 1-3 Yamadaoka, Suita, Osaka, 565-0871, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22323812" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cell Communication ; Cell Movement ; Cells, Cultured ; Chromatophores/*physiology ; Melanophores/*physiology ; Membrane Potentials ; Mutation ; Skin/cytology ; *Skin Pigmentation ; Zebrafish/*anatomy & histology/physiology
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    Crystal structure of the heterodimeric CLOCK:BMAL1 transcriptional activator complex (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-06-02
    Description: The circadian clock in mammals is driven by an autoregulatory transcriptional feedback mechanism that takes approximately 24 hours to complete. A key component of this mechanism is a heterodimeric transcriptional activator consisting of two basic helix-loop-helix PER-ARNT-SIM (bHLH-PAS) domain protein subunits, CLOCK and BMAL1. Here, we report the crystal structure of a complex containing the mouse CLOCK:BMAL1 bHLH-PAS domains at 2.3 A resolution. The structure reveals an unusual asymmetric heterodimer with the three domains in each of the two subunits--bHLH, PAS-A, and PAS-B--tightly intertwined and involved in dimerization interactions, resulting in three distinct protein interfaces. Mutations that perturb the observed heterodimer interfaces affect the stability and activity of the CLOCK:BMAL1 complex as well as the periodicity of the circadian oscillator. The structure of the CLOCK:BMAL1 complex is a starting point for understanding at an atomic level the mechanism driving the mammalian circadian clock.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694778/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3694778/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Huang, Nian -- Chelliah, Yogarany -- Shan, Yongli -- Taylor, Clinton A -- Yoo, Seung-Hee -- Partch, Carrie -- Green, Carla B -- Zhang, Hong -- Takahashi, Joseph S -- R01 GM081875/GM/NIGMS NIH HHS/ -- R01 GM090247/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Jul 13;337(6091):189-94. doi: 10.1126/science.1222804. Epub 2012 May 31.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biochemistry, University of Texas Southwestern Medical Center, Dallas, TX 75390, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22653727" target="_blank"〉PubMed〈/a〉
    Keywords: ARNTL Transcription Factors/*chemistry/genetics/metabolism ; Amino Acid Sequence ; Animals ; CLOCK Proteins/*chemistry/genetics/metabolism ; Cells, Cultured ; *Circadian Rhythm ; Crystallography, X-Ray ; DNA/metabolism ; HEK293 Cells ; Helix-Loop-Helix Motifs ; Humans ; Mice ; Models, Molecular ; Molecular Sequence Data ; Mutant Proteins/chemistry/metabolism ; Protein Binding ; Protein Interaction Domains and Motifs ; Protein Multimerization ; Protein Structure, Quaternary ; Protein Structure, Secondary ; Protein Structure, Tertiary ; Protein Subunits/chemistry/metabolism ; Static Electricity ; *Transcriptional Activation
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    IRE1alpha cleaves select microRNAs during ER stress to derepress translation of proapoptotic Caspase-2 (2012)
    American Association for the Advancement of Science (AAAS)
    Details
    Publication Date: 2012-10-09
    Description: The endoplasmic reticulum (ER) is the primary organelle for folding and maturation of secretory and transmembrane proteins. Inability to meet protein-folding demand leads to "ER stress," and activates IRE1alpha, an ER transmembrane kinase-endoribonuclease (RNase). IRE1alpha promotes adaptation through splicing Xbp1 mRNA or apoptosis through incompletely understood mechanisms. Here, we found that sustained IRE1alpha RNase activation caused rapid decay of select microRNAs (miRs -17, -34a, -96, and -125b) that normally repress translation of Caspase-2 mRNA, and thus sharply elevates protein levels of this initiator protease of the mitochondrial apoptotic pathway. In cell-free systems, recombinant IRE1alpha endonucleolytically cleaved microRNA precursors at sites distinct from DICER. Thus, IRE1alpha regulates translation of a proapoptotic protein through terminating microRNA biogenesis, and noncoding RNAs are part of the ER stress response.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742121/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3742121/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Upton, John-Paul -- Wang, Likun -- Han, Dan -- Wang, Eric S -- Huskey, Noelle E -- Lim, Lionel -- Truitt, Morgan -- McManus, Michael T -- Ruggero, Davide -- Goga, Andrei -- Papa, Feroz R -- Oakes, Scott A -- DK063720/DK/NIDDK NIH HHS/ -- DP2 OD001925/OD/NIH HHS/ -- DP2OD001925/OD/NIH HHS/ -- GM080783/GM/NIGMS NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- R01 CA136577/CA/NCI NIH HHS/ -- R01 CA136717/CA/NCI NIH HHS/ -- R01 CA140456/CA/NCI NIH HHS/ -- R01 CA154916/CA/NCI NIH HHS/ -- R01 DK080955/DK/NIDDK NIH HHS/ -- R01 GM080783/GM/NIGMS NIH HHS/ -- R01CA136577/CA/NCI NIH HHS/ -- R01CA136717/CA/NCI NIH HHS/ -- R01CA140456/CA/NCI NIH HHS/ -- R01CA154916/CA/NCI NIH HHS/ -- R01DK080955/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2012 Nov 9;338(6108):818-22. doi: 10.1126/science.1226191. Epub 2012 Oct 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Pathology, University of California, San Francisco, San Francisco, CA 94143, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23042294" target="_blank"〉PubMed〈/a〉
    Keywords: 3' Untranslated Regions ; Animals ; Apoptosis ; Brefeldin A/pharmacology ; Caspase 2/*genetics/*metabolism ; Cell-Free System ; Cells, Cultured ; Cysteine Endopeptidases/*genetics/*metabolism ; Down-Regulation ; Endoplasmic Reticulum/metabolism ; *Endoplasmic Reticulum Stress ; Endoribonucleases/chemistry/genetics/*metabolism ; Enzyme Activation ; HEK293 Cells ; Humans ; Mice ; Mice, Knockout ; MicroRNAs/*metabolism ; Mutant Proteins ; Protein Biosynthesis ; Protein-Serine-Threonine Kinases/chemistry/genetics/*metabolism ; RNA Stability ; RNA, Messenger/genetics/metabolism ; Up-Regulation
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    Removal of shelterin reveals the telomere end-protection problem (2012)
    American Association for the Advancement of Science (AAAS)
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    Publication Date: 2012-05-05
    Description: The telomere end-protection problem is defined by the aggregate of DNA damage signaling and repair pathways that require repression at telomeres. To define the end-protection problem, we removed the whole shelterin complex from mouse telomeres through conditional deletion of TRF1 and TRF2 in nonhomologous end-joining (NHEJ) deficient cells. The data reveal two DNA damage response pathways not previously observed upon deletion of individual shelterin proteins. The shelterin-free telomeres are processed by microhomology-mediated alternative-NHEJ when Ku70/80 is absent and are attacked by nucleolytic degradation in the absence of 53BP1. The data establish that the end-protection problem is specified by six pathways [ATM (ataxia telangiectasia mutated) and ATR (ataxia telangiectasia and Rad3 related) signaling, classical-NHEJ, alt-NHEJ, homologous recombination, and resection] and show how shelterin acts with general DNA damage response factors to solve this problem.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3477646/" target="_blank"〉〈img src="https://static.pubmed.gov/portal/portal3rc.fcgi/4089621/img/3977009" border="0"〉〈/a〉   〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3477646/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sfeir, Agnel -- de Lange, Titia -- AG016642/AG/NIA NIH HHS/ -- GM49046/GM/NIGMS NIH HHS/ -- R01 AG016642/AG/NIA NIH HHS/ -- R01 CA076027/CA/NCI NIH HHS/ -- R37 GM049046/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2012 May 4;336(6081):593-7. doi: 10.1126/science.1218498.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Laboratory for Cell Biology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/22556254" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Antigens, Nuclear/genetics/metabolism ; Ataxia Telangiectasia Mutated Proteins ; Cell Cycle ; Cell Cycle Proteins/metabolism ; Cells, Cultured ; Chromosomal Proteins, Non-Histone/metabolism ; DNA Breaks, Double-Stranded ; DNA End-Joining Repair ; DNA Ligases/metabolism ; DNA Repair ; DNA-Binding Proteins/genetics/metabolism ; Homologous Recombination ; Mice ; Mice, Knockout ; Poly(ADP-ribose) Polymerases/metabolism ; Protein-Serine-Threonine Kinases/metabolism ; Signal Transduction ; Telomere/*metabolism/ultrastructure ; *Telomere Homeostasis ; Telomere-Binding Proteins/genetics/*metabolism ; Telomeric Repeat Binding Protein 1/genetics/metabolism ; Telomeric Repeat Binding Protein 2/genetics/metabolism ; Tumor Suppressor Proteins/metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
    Published by American Association for the Advancement of Science (AAAS)
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