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  • 1
    Series available for loan
    Series available for loan
    Butte, Mont.
    Associated volumes
    Call number: MR 90.1012
    In: Bulletin
    Type of Medium: Series available for loan
    Pages: VI, 53 S. + 1 Beil.
    Edition: 1st print.
    Series Statement: Bulletin / Montana Bureau of Mines and Geology 115
    Language: English
    Location: Lower compact magazine
    Branch Library: GFZ Library
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  • 2
    Publication Date: 2015-04-28
    Description: Motivation: RNA-Seq is a method for profiling transcription using high-throughput sequencing and is an important component of many research projects that wish to study transcript isoforms, condition specific expression and transcriptional structure. The methods, tools and technologies used to perform RNA-Seq analysis continue to change, creating a bioinformatics challenge for researchers who wish to exploit these data. Resources that bring together genomic data, analysis tools, educational material and computational infrastructure can minimize the overhead required of life science researchers. Results: RNA-Rocket is a free service that provides access to RNA-Seq and ChIP-Seq analysis tools for studying infectious diseases. The site makes available thousands of pre-indexed genomes, their annotations and the ability to stream results to the bioinformatics resources VectorBase, EuPathDB and PATRIC. The site also provides a combination of experimental data and metadata, examples of pre-computed analysis, step-by-step guides and a user interface designed to enable both novice and experienced users of RNA-Seq data. Availability and implementation: RNA-Rocket is available at rnaseq.pathogenportal.org. Source code for this project can be found at github.com/cidvbi/PathogenPortal. Contact: anwarren@vt.edu Supplementary information: Supplementary materials are available at Bioinformatics online.
    Print ISSN: 1367-4803
    Electronic ISSN: 1460-2059
    Topics: Biology , Computer Science , Medicine
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  • 3
    Publication Date: 2012-04-25
    Description: Suppression of cyclooxygenase 2 (COX-2)–derived prostacyclin (PGI2) is sufficient to explain most elements of the cardiovascular hazard from nonsteroidal antinflammatory drugs (NSAIDs). However, randomized trials are consistent with the emergence of cardiovascular risk during chronic dosing with NSAIDs. Although deletion of the PGI2 receptor fosters atherogenesis, the importance of COX-2 during development has constrained the use of conventional knockout (KO) mice to address this question. We developed mice in which COX-2 was deleted postnatally, bypassing cardiorenal defects exhibited by conventional KOs. When crossed into ApoE-deficient hyperlipidemic mice, COX-2 deletion accelerated atherogenesis in both genders, with lesions exhibiting leukocyte infiltration and phenotypic modulation of vascular smooth muscle cells, as reflected by loss of α-smooth muscle cell actin and up-regulation of vascular cell adhesion molecule-1. Stimulated peritoneal macrophages revealed suppression of COX-2–derived prostanoids and augmented 5-lipoxygenase product formation, consistent with COX-2 substrate rediversion. Although deletion of the 5-lipoxygenase activating protein (FLAP) did not influence atherogenesis, it attenuated the proatherogeneic impact of COX-2 deletion in hyperlipidemic mice. Chronic administration of NSAIDs may increasingly confer a cardiovascular hazard on patients at low initial risk. Promotion of atherogenesis by postnatal COX-2 deletion affords a mechanistic explanation for this observation. Coincident inhibition of FLAP may offer an approach to attenuating such a risk from NSAIDs.
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
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  • 4
    Publication Date: 2010-04-07
    Description: Within the circulatory system, blood flow regulates vascular remodelling, stimulates blood stem cell formation, and has a role in the pathology of vascular disease. During vertebrate embryogenesis, vascular patterning is initially guided by conserved genetic pathways that act before circulation. Subsequently, endothelial cells must incorporate the mechanosensory stimulus of blood flow with these early signals to shape the embryonic vascular system. However, few details are known about how these signals are integrated during development. To investigate this process, we focused on the aortic arch (AA) blood vessels, which are known to remodel in response to blood flow. By using two-photon imaging of live zebrafish embryos, we observe that flow is essential for angiogenesis during AA development. We further find that angiogenic sprouting of AA vessels requires a flow-induced genetic pathway in which the mechano-sensitive zinc finger transcription factor klf2a induces expression of an endothelial-specific microRNA, mir-126, to activate Vegf signalling. Taken together, our work describes a novel genetic mechanism in which a microRNA facilitates integration of a physiological stimulus with growth factor signalling in endothelial cells to guide angiogenesis.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2914488/" 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/PMC2914488/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nicoli, Stefania -- Standley, Clive -- Walker, Paul -- Hurlstone, Adam -- Fogarty, Kevin E -- Lawson, Nathan D -- DK32520/DK/NIDDK NIH HHS/ -- R01 CA107454/CA/NCI NIH HHS/ -- R01 CA107454-05/CA/NCI NIH HHS/ -- R01 HL079266/HL/NHLBI NIH HHS/ -- R01 HL079266-05/HL/NHLBI NIH HHS/ -- England -- Nature. 2010 Apr 22;464(7292):1196-200. doi: 10.1038/nature08889. Epub 2010 Apr 4.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Program in Gene Function and Expression, University of Massachusetts Medical School, Worcester, Massachusetts 01605, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20364122" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Aorta, Thoracic/*embryology ; Endothelial Cells/metabolism ; Gene Expression Regulation, Developmental ; *Hemodynamics ; Intracellular Signaling Peptides and Proteins/genetics/metabolism ; Kruppel-Like Transcription Factors/metabolism ; Membrane Proteins/genetics/metabolism ; Mice ; MicroRNAs/genetics/*metabolism ; NIH 3T3 Cells ; *Neovascularization, Physiologic ; Regional Blood Flow/physiology ; *Signal Transduction ; Vascular Endothelial Growth Factor A/*metabolism ; Zebrafish/blood/embryology/*genetics ; Zebrafish Proteins/genetics/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
    Publication Date: 2010-05-08
    Description: Dicer is a central enzyme in microRNA (miRNA) processing. We identified a Dicer-independent miRNA biogenesis pathway that uses Argonaute2 (Ago2) slicer catalytic activity. In contrast to other miRNAs, miR-451 levels were refractory to dicer loss of function but were reduced in MZago2 (maternal-zygotic) mutants. We found that pre-miR-451 processing requires Ago2 catalytic activity in vivo. MZago2 mutants showed delayed erythropoiesis that could be rescued by wild-type Ago2 or miR-451-duplex but not by catalytically dead Ago2. Changing the secondary structure of Dicer-dependent miRNAs to mimic that of pre-miR-451 restored miRNA function and rescued developmental defects in MZdicer mutants, indicating that the pre-miRNA secondary structure determines the processing pathway in vivo. We propose that Ago2-mediated cleavage of pre-miRNAs, followed by uridylation and trimming, generates functional miRNAs independently of Dicer.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3093307/" 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/PMC3093307/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Cifuentes, Daniel -- Xue, Huiling -- Taylor, David W -- Patnode, Heather -- Mishima, Yuichiro -- Cheloufi, Sihem -- Ma, Enbo -- Mane, Shrikant -- Hannon, Gregory J -- Lawson, Nathan D -- Wolfe, Scot A -- Giraldez, Antonio J -- P01 CA013106/CA/NCI NIH HHS/ -- P01 CA013106-38/CA/NCI NIH HHS/ -- R01 GM081602/GM/NIGMS NIH HHS/ -- R01 GM081602-01/GM/NIGMS NIH HHS/ -- R01 GM081602-02/GM/NIGMS NIH HHS/ -- R01 GM081602-03/GM/NIGMS NIH HHS/ -- R01 GM081602-03S1/GM/NIGMS NIH HHS/ -- R01 GM081602-04/GM/NIGMS NIH HHS/ -- R01 GM101108/GM/NIGMS NIH HHS/ -- R01 HL093766/HL/NHLBI NIH HHS/ -- R01 HL093766-04/HL/NHLBI NIH HHS/ -- R01GM081602-03/03S1/GM/NIGMS NIH HHS/ -- R01HL093766/HL/NHLBI NIH HHS/ -- Howard Hughes Medical Institute/ -- New York, N.Y. -- Science. 2010 Jun 25;328(5986):1694-8. doi: 10.1126/science.1190809. Epub 2010 May 6.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Genetics, Yale University School of Medicine, New Haven, CT 06510, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20448148" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Argonaute Proteins ; Biocatalysis ; Embryo, Nonmammalian/metabolism ; Embryonic Development ; Erythropoiesis ; Eukaryotic Initiation Factor-2/genetics/*metabolism ; Humans ; MicroRNAs/*chemistry/*metabolism ; Models, Biological ; Morphogenesis ; Nucleic Acid Conformation ; RNA Precursors/metabolism ; RNA Processing, Post-Transcriptional ; Recombinant Proteins/metabolism ; Ribonuclease III/metabolism ; Zebrafish/embryology/genetics/*metabolism ; Zebrafish Proteins/genetics/*metabolism
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 6
    Publication Date: 2011-06-10
    Description: Haematopoietic stem cells (HSCs) are a self-renewing population of cells that continuously replenish all blood and immune cells during the lifetime of an individual. HSCs are used clinically to treat a wide array of diseases, including acute leukaemias and congenital blood disorders, but obtaining suitable numbers of cells and finding immune-compatible donors remain serious problems. These difficulties have led to an interest in the conversion of embryonic stem cells or induced pluripotent stem cells into HSCs, which is not possible using current methodologies. To accomplish this goal, it is critical to understand the native mechanisms involved in the specification of HSCs during embryonic development. Here we demonstrate in zebrafish that Wnt16 controls a novel genetic regulatory network required for HSC specification. Non-canonical signalling by Wnt16 is required for somitic expression of the Notch ligands deltaC (dlc) and deltaD (dld), and these ligands are, in turn, required for the establishment of definitive haematopoiesis. Notch signalling downstream of Dlc and Dld is earlier than, and distinct from, known cell-autonomous requirements for Notch, strongly suggesting that novel Notch-dependent relay signal(s) induce the first HSCs in parallel to other established pathways. Our results demonstrate that somite-specific gene expression is required for the production of haemogenic endothelium.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3304471/" 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/PMC3304471/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Clements, Wilson K -- Kim, Albert D -- Ong, Karen G -- Moore, John C -- Lawson, Nathan D -- Traver, David -- R01 DK074482/DK/NIDDK NIH HHS/ -- R01 DK074482-05/DK/NIDDK NIH HHS/ -- R01-DK074482/DK/NIDDK NIH HHS/ -- R01-HL093467/HL/NHLBI NIH HHS/ -- England -- Nature. 2011 Jun 8;474(7350):220-4. doi: 10.1038/nature10107.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Cellular and Molecular Medicine and Section of Cell and Developmental Biology, University of California at San Diego, 9500 Gilman Drive, La Jolla, California 92093-0380, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/21654806" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Cell Differentiation ; Cell Lineage ; Hematopoiesis ; Hematopoietic Stem Cells/*cytology/*metabolism ; Intracellular Signaling Peptides and Proteins ; Ligands ; Membrane Proteins/metabolism ; Nerve Tissue Proteins/metabolism ; Phenotype ; Receptors, Notch/*metabolism ; *Signal Transduction ; Somites/cytology/*metabolism ; Wnt Proteins/deficiency/genetics/*metabolism ; Zebrafish/*metabolism ; Zebrafish Proteins/deficiency/genetics/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 7
    Publication Date: 2015-09-15
    Description: The contribution of rare and low-frequency variants to human traits is largely unexplored. Here we describe insights from sequencing whole genomes (low read depth, 7x) or exomes (high read depth, 80x) of nearly 10,000 individuals from population-based and disease collections. In extensively phenotyped cohorts we characterize over 24 million novel sequence variants, generate a highly accurate imputation reference panel and identify novel alleles associated with levels of triglycerides (APOB), adiponectin (ADIPOQ) and low-density lipoprotein cholesterol (LDLR and RGAG1) from single-marker and rare variant aggregation tests. We describe population structure and functional annotation of rare and low-frequency variants, use the data to estimate the benefits of sequencing for association studies, and summarize lessons from disease-specific collections. Finally, we make available an extensive resource, including individual-level genetic and phenotypic data and web-based tools to facilitate the exploration of association results.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4773891/" 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/PMC4773891/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉UK10K Consortium -- Walter, Klaudia -- Min, Josine L -- Huang, Jie -- Crooks, Lucy -- Memari, Yasin -- McCarthy, Shane -- Perry, John R B -- Xu, ChangJiang -- Futema, Marta -- Lawson, Daniel -- Iotchkova, Valentina -- Schiffels, Stephan -- Hendricks, Audrey E -- Danecek, Petr -- Li, Rui -- Floyd, James -- Wain, Louise V -- Barroso, Ines -- Humphries, Steve E -- Hurles, Matthew E -- Zeggini, Eleftheria -- Barrett, Jeffrey C -- Plagnol, Vincent -- Richards, J Brent -- Greenwood, Celia M T -- Timpson, Nicholas J -- Durbin, Richard -- Soranzo, Nicole -- 091551/Wellcome Trust/United Kingdom -- 095515/Wellcome Trust/United Kingdom -- 095564/Wellcome Trust/United Kingdom -- 098498/Wellcome Trust/United Kingdom -- 100140/Wellcome Trust/United Kingdom -- 104036/Wellcome Trust/United Kingdom -- CZD/16/6/4/Chief Scientist Office/United Kingdom -- MC_UU_12013/3/Medical Research Council/United Kingdom -- RG/10/13/28570/British Heart Foundation/United Kingdom -- WT091310/Wellcome Trust/United Kingdom -- England -- Nature. 2015 Oct 1;526(7571):82-90. doi: 10.1038/nature14962. Epub 2015 Sep 14.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/26367797" target="_blank"〉PubMed〈/a〉
    Keywords: Adiponectin/blood ; Alleles ; Cohort Studies ; Disease/*genetics ; Exome/genetics ; Female ; Genetic Predisposition to Disease/genetics ; Genetic Variation/*genetics ; Genetics, Medical ; Genetics, Population ; Genome, Human/*genetics ; Genome-Wide Association Study ; Genomics ; Great Britain ; *Health ; Humans ; Lipid Metabolism/genetics ; Male ; Molecular Sequence Annotation ; Receptors, LDL/genetics ; Reference Standards ; Sequence Analysis, DNA ; Triglycerides/blood
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
    Publication Date: 2007-05-19
    Description: We present a draft sequence of the genome of Aedes aegypti, the primary vector for yellow fever and dengue fever, which at approximately 1376 million base pairs is about 5 times the size of the genome of the malaria vector Anopheles gambiae. Nearly 50% of the Ae. aegypti genome consists of transposable elements. These contribute to a factor of approximately 4 to 6 increase in average gene length and in sizes of intergenic regions relative to An. gambiae and Drosophila melanogaster. Nonetheless, chromosomal synteny is generally maintained among all three insects, although conservation of orthologous gene order is higher (by a factor of approximately 2) between the mosquito species than between either of them and the fruit fly. An increase in genes encoding odorant binding, cytochrome P450, and cuticle domains relative to An. gambiae suggests that members of these protein families underpin some of the biological differences between the two mosquito species.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2868357/" 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/PMC2868357/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nene, Vishvanath -- Wortman, Jennifer R -- Lawson, Daniel -- Haas, Brian -- Kodira, Chinnappa -- Tu, Zhijian Jake -- Loftus, Brendan -- Xi, Zhiyong -- Megy, Karyn -- Grabherr, Manfred -- Ren, Quinghu -- Zdobnov, Evgeny M -- Lobo, Neil F -- Campbell, Kathryn S -- Brown, Susan E -- Bonaldo, Maria F -- Zhu, Jingsong -- Sinkins, Steven P -- Hogenkamp, David G -- Amedeo, Paolo -- Arensburger, Peter -- Atkinson, Peter W -- Bidwell, Shelby -- Biedler, Jim -- Birney, Ewan -- Bruggner, Robert V -- Costas, Javier -- Coy, Monique R -- Crabtree, Jonathan -- Crawford, Matt -- Debruyn, Becky -- Decaprio, David -- Eiglmeier, Karin -- Eisenstadt, Eric -- El-Dorry, Hamza -- Gelbart, William M -- Gomes, Suely L -- Hammond, Martin -- Hannick, Linda I -- Hogan, James R -- Holmes, Michael H -- Jaffe, David -- Johnston, J Spencer -- Kennedy, Ryan C -- Koo, Hean -- Kravitz, Saul -- Kriventseva, Evgenia V -- Kulp, David -- Labutti, Kurt -- Lee, Eduardo -- Li, Song -- Lovin, Diane D -- Mao, Chunhong -- Mauceli, Evan -- Menck, Carlos F M -- Miller, Jason R -- Montgomery, Philip -- Mori, Akio -- Nascimento, Ana L -- Naveira, Horacio F -- Nusbaum, Chad -- O'leary, Sinead -- Orvis, Joshua -- Pertea, Mihaela -- Quesneville, Hadi -- Reidenbach, Kyanne R -- Rogers, Yu-Hui -- Roth, Charles W -- Schneider, Jennifer R -- Schatz, Michael -- Shumway, Martin -- Stanke, Mario -- Stinson, Eric O -- Tubio, Jose M C -- Vanzee, Janice P -- Verjovski-Almeida, Sergio -- Werner, Doreen -- White, Owen -- Wyder, Stefan -- Zeng, Qiandong -- Zhao, Qi -- Zhao, Yongmei -- Hill, Catherine A -- Raikhel, Alexander S -- Soares, Marcelo B -- Knudson, Dennis L -- Lee, Norman H -- Galagan, James -- Salzberg, Steven L -- Paulsen, Ian T -- Dimopoulos, George -- Collins, Frank H -- Birren, Bruce -- Fraser-Liggett, Claire M -- Severson, David W -- 079059/Wellcome Trust/United Kingdom -- 5 R01 AI61576-2/AI/NIAID NIH HHS/ -- R01 AI059492/AI/NIAID NIH HHS/ -- R01 LM006845/LM/NLM NIH HHS/ -- R01 LM006845-08/LM/NLM NIH HHS/ -- R37 AI024716/AI/NIAID NIH HHS/ -- UO1 AI50936/AI/NIAID NIH HHS/ -- New York, N.Y. -- Science. 2007 Jun 22;316(5832):1718-23. Epub 2007 May 17.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute for Genomic Research, 9712 Medical Center Drive, Rockville, MD 20850, USA. nene@tigr.org〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/17510324" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/*genetics/metabolism ; Animals ; Anopheles gambiae/genetics/metabolism ; Arboviruses ; Base Sequence ; DNA Transposable Elements ; Dengue/prevention & control/transmission ; Drosophila melanogaster/genetics ; Female ; Genes, Insect ; *Genome, Insect ; Humans ; Insect Proteins/genetics ; Insect Vectors/*genetics/metabolism ; Male ; Membrane Transport Proteins/genetics ; Molecular Sequence Data ; Multigene Family ; Protein Structure, Tertiary/genetics ; Sequence Analysis, DNA ; Sex Characteristics ; Sex Determination Processes ; Species Specificity ; Synteny ; Transcription, Genetic ; Yellow Fever/prevention & control/transmission
    Print ISSN: 0036-8075
    Electronic ISSN: 1095-9203
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  • 9
    Publication Date: 2010-10-23
    Description: The Afrotropical mosquito Anopheles gambiae sensu stricto, a major vector of malaria, is currently undergoing speciation into the M and S molecular forms. These forms have diverged in larval ecology and reproductive behavior through unknown genetic mechanisms, despite considerable levels of hybridization. Previous genome-wide scans using gene-based microarrays uncovered divergence between M and S that was largely confined to gene-poor pericentromeric regions, prompting a speciation-with-ongoing-gene-flow model that implicated only about 3% of the genome near centromeres in the speciation process. Here, based on the complete M and S genome sequences, we report widespread and heterogeneous genomic divergence inconsistent with appreciable levels of interform gene flow, suggesting a more advanced speciation process and greater challenges to identify genes critical to initiating that process.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674514/" 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/PMC3674514/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Lawniczak, M K N -- Emrich, S J -- Holloway, A K -- Regier, A P -- Olson, M -- White, B -- Redmond, S -- Fulton, L -- Appelbaum, E -- Godfrey, J -- Farmer, C -- Chinwalla, A -- Yang, S-P -- Minx, P -- Nelson, J -- Kyung, K -- Walenz, B P -- Garcia-Hernandez, E -- Aguiar, M -- Viswanathan, L D -- Rogers, Y-H -- Strausberg, R L -- Saski, C A -- Lawson, D -- Collins, F H -- Kafatos, F C -- Christophides, G K -- Clifton, S W -- Kirkness, E F -- Besansky, N J -- AI076584/AI/NIAID NIH HHS/ -- BB/C519670/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- BB/E002641/1/Biotechnology and Biological Sciences Research Council/United Kingdom -- R01 AI063508/AI/NIAID NIH HHS/ -- R01 AI076584/AI/NIAID NIH HHS/ -- R01 AI63508/AI/NIAID NIH HHS/ -- U54-HG00379/HG/NHGRI NIH HHS/ -- U54-HG03068/HG/NHGRI NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 22;330(6003):512-4. doi: 10.1126/science.1195755.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Division of Cell and Molecular Biology, Imperial College London, South Kensington Campus, London SW7 2AZ, UK.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20966253" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anopheles gambiae/classification/*genetics ; Evolution, Molecular ; Female ; Gene Flow ; *Genetic Speciation ; *Genome, Insect ; Male ; Models, Genetic ; Polymorphism, Single Nucleotide
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    Electronic ISSN: 1095-9203
    Topics: Biology , Chemistry and Pharmacology , Computer Science , Medicine , Natural Sciences in General , Physics
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  • 10
    Publication Date: 2010-10-12
    Description: Culex quinquefasciatus (the southern house mosquito) is an important mosquito vector of viruses such as West Nile virus and St. Louis encephalitis virus, as well as of nematodes that cause lymphatic filariasis. C. quinquefasciatus is one species within the Culex pipiens species complex and can be found throughout tropical and temperate climates of the world. The ability of C. quinquefasciatus to take blood meals from birds, livestock, and humans contributes to its ability to vector pathogens between species. Here, we describe the genomic sequence of C. quinquefasciatus: Its repertoire of 18,883 protein-coding genes is 22% larger than that of Aedes aegypti and 52% larger than that of Anopheles gambiae with multiple gene-family expansions, including olfactory and gustatory receptors, salivary gland genes, and genes associated with xenobiotic detoxification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3740384/" 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/PMC3740384/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Arensburger, Peter -- Megy, Karine -- Waterhouse, Robert M -- Abrudan, Jenica -- Amedeo, Paolo -- Antelo, Beatriz -- Bartholomay, Lyric -- Bidwell, Shelby -- Caler, Elisabet -- Camara, Francisco -- Campbell, Corey L -- Campbell, Kathryn S -- Casola, Claudio -- Castro, Marta T -- Chandramouliswaran, Ishwar -- Chapman, Sinead B -- Christley, Scott -- Costas, Javier -- Eisenstadt, Eric -- Feschotte, Cedric -- Fraser-Liggett, Claire -- Guigo, Roderic -- Haas, Brian -- Hammond, Martin -- Hansson, Bill S -- Hemingway, Janet -- Hill, Sharon R -- Howarth, Clint -- Ignell, Rickard -- Kennedy, Ryan C -- Kodira, Chinnappa D -- Lobo, Neil F -- Mao, Chunhong -- Mayhew, George -- Michel, Kristin -- Mori, Akio -- Liu, Nannan -- Naveira, Horacio -- Nene, Vishvanath -- Nguyen, Nam -- Pearson, Matthew D -- Pritham, Ellen J -- Puiu, Daniela -- Qi, Yumin -- Ranson, Hilary -- Ribeiro, Jose M C -- Roberston, Hugh M -- Severson, David W -- Shumway, Martin -- Stanke, Mario -- Strausberg, Robert L -- Sun, Cheng -- Sutton, Granger -- Tu, Zhijian Jake -- Tubio, Jose Manuel C -- Unger, Maria F -- Vanlandingham, Dana L -- Vilella, Albert J -- White, Owen -- White, Jared R -- Wondji, Charles S -- Wortman, Jennifer -- Zdobnov, Evgeny M -- Birren, Bruce -- Christensen, Bruce M -- Collins, Frank H -- Cornel, Anthony -- Dimopoulos, George -- Hannick, Linda I -- Higgs, Stephen -- Lanzaro, Gregory C -- Lawson, Daniel -- Lee, Norman H -- Muskavitch, Marc A T -- Raikhel, Alexander S -- Atkinson, Peter W -- HHSN266200400001C/PHS HHS/ -- HHSN266200400039C/AI/NIAID NIH HHS/ -- HHSN266200400039C/PHS HHS/ -- N01-AI-30071/AI/NIAID NIH HHS/ -- N01AI30071/AI/NIAID NIH HHS/ -- ZIA AI000810-13/Intramural NIH HHS/ -- New York, N.Y. -- Science. 2010 Oct 1;330(6000):86-8. doi: 10.1126/science.1191864.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Center for Disease Vector Research, University of California Riverside, Riverside, CA 92521, USA. arensburger@gmail.com〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929810" target="_blank"〉PubMed〈/a〉
    Keywords: Aedes/genetics ; Animals ; Anopheles gambiae/genetics ; Chromosome Mapping ; Chromosomes/*genetics ; Culex/classification/*genetics/physiology ; DNA Transposable Elements ; *Genes, Insect ; *Genome ; Insect Proteins/genetics/physiology ; Insect Vectors/genetics ; Molecular Sequence Data ; Multigene Family ; Phylogeny ; Receptors, Odorant/genetics ; Retroelements ; *Sequence Analysis, DNA
    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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