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  • Articles  (133)
  • Mice, Inbred C57BL  (133)
  • Nature Publishing Group (NPG)  (133)
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  • Articles  (133)
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  • 2010-2014  (133)
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  • 1
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    A synaptic and circuit basis for corollary discharge in the auditory cortex (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-08-28
    Description: Sensory regions of the brain integrate environmental cues with copies of motor-related signals important for imminent and ongoing movements. In mammals, signals propagating from the motor cortex to the auditory cortex are thought to have a critical role in normal hearing and behaviour, yet the synaptic and circuit mechanisms by which these motor-related signals influence auditory cortical activity remain poorly understood. Using in vivo intracellular recordings in behaving mice, we find that excitatory neurons in the auditory cortex are suppressed before and during movement, owing in part to increased activity of local parvalbumin-positive interneurons. Electrophysiology and optogenetic gain- and loss-of-function experiments reveal that motor-related changes in auditory cortical dynamics are driven by a subset of neurons in the secondary motor cortex that innervate the auditory cortex and are active during movement. These findings provide a synaptic and circuit basis for the motor-related corollary discharge hypothesized to facilitate hearing and auditory-guided behaviours.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4248668/" 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/PMC4248668/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Schneider, David M -- Nelson, Anders -- Mooney, Richard -- NS079929/NS/NINDS NIH HHS/ -- R01 DC013826/DC/NIDCD NIH HHS/ -- R21 NS079929/NS/NINDS NIH HHS/ -- T32 GM008441/GM/NIGMS NIH HHS/ -- England -- Nature. 2014 Sep 11;513(7517):189-94. doi: 10.1038/nature13724. Epub 2014 Aug 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Department of Neurobiology, Duke University School of Medicine, Durham, North Carolina 27710, USA [2]. ; Department of Neurobiology, Duke University School of Medicine, Durham, North Carolina 27710, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25162524" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Auditory Cortex/*physiology ; Electrical Synapses/*physiology ; Female ; Male ; Mice ; Mice, Inbred C57BL ; Motor Activity/*physiology ; Optogenetics ; Sensory Receptor Cells/metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 2
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    Deubiquitinase DUBA is a post-translational brake on interleukin-17 production in T cells (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-12-04
    Description: T-helper type 17 (TH17) cells that produce the cytokines interleukin-17A (IL-17A) and IL-17F are implicated in the pathogenesis of several autoimmune diseases. The differentiation of TH17 cells is regulated by transcription factors such as RORgammat, but post-translational mechanisms preventing the rampant production of pro-inflammatory IL-17A have received less attention. Here we show that the deubiquitylating enzyme DUBA is a negative regulator of IL-17A production in T cells. Mice with DUBA-deficient T cells developed exacerbated inflammation in the small intestine after challenge with anti-CD3 antibodies. DUBA interacted with the ubiquitin ligase UBR5, which suppressed DUBA abundance in naive T cells. DUBA accumulated in activated T cells and stabilized UBR5, which then ubiquitylated RORgammat in response to TGF-beta signalling. Our data identify DUBA as a cell-intrinsic suppressor of IL-17 production.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Rutz, Sascha -- Kayagaki, Nobuhiko -- Phung, Qui T -- Eidenschenk, Celine -- Noubade, Rajkumar -- Wang, Xiaoting -- Lesch, Justin -- Lu, Rongze -- Newton, Kim -- Huang, Oscar W -- Cochran, Andrea G -- Vasser, Mark -- Fauber, Benjamin P -- DeVoss, Jason -- Webster, Joshua -- Diehl, Lauri -- Modrusan, Zora -- Kirkpatrick, Donald S -- Lill, Jennie R -- Ouyang, Wenjun -- Dixit, Vishva M -- England -- Nature. 2015 Feb 19;518(7539):417-21. doi: 10.1038/nature13979. Epub 2014 Dec 3.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Immunology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Physiological Chemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Protein Chemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Early Discovery Biochemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Discovery Chemistry, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Pathology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA. ; Department of Molecular Biology, Genentech, 1 DNA Way, South San Francisco, California 94080, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25470037" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Enzyme Stability ; Female ; Inflammation/genetics/pathology ; Interleukin-17/*biosynthesis ; Intestine, Small/metabolism/pathology ; Lymphocyte Activation ; Mice ; Mice, Inbred C57BL ; Nuclear Receptor Subfamily 1, Group F, Member 3/metabolism ; Proteasome Endopeptidase Complex/metabolism ; Protein Binding ; *Protein Biosynthesis ; Signal Transduction ; Substrate Specificity ; Th17 Cells/*metabolism ; Transforming Growth Factor beta/metabolism ; Ubiquitin-Protein Ligases/metabolism ; Ubiquitin-Specific Proteases/biosynthesis/deficiency/genetics/*metabolism ; Ubiquitination
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 3
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    Precision microbiome reconstitution restores bile acid mediated resistance to Clostridium difficile (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-10-23
    Description: The gastrointestinal tracts of mammals are colonized by hundreds of microbial species that contribute to health, including colonization resistance against intestinal pathogens. Many antibiotics destroy intestinal microbial communities and increase susceptibility to intestinal pathogens. Among these, Clostridium difficile, a major cause of antibiotic-induced diarrhoea, greatly increases morbidity and mortality in hospitalized patients. Which intestinal bacteria provide resistance to C. difficile infection and their in vivo inhibitory mechanisms remain unclear. Here we correlate loss of specific bacterial taxa with development of infection, by treating mice with different antibiotics that result in distinct microbiota changes and lead to varied susceptibility to C. difficile. Mathematical modelling augmented by analyses of the microbiota of hospitalized patients identifies resistance-associated bacteria common to mice and humans. Using these platforms, we determine that Clostridium scindens, a bile acid 7alpha-dehydroxylating intestinal bacterium, is associated with resistance to C. difficile infection and, upon administration, enhances resistance to infection in a secondary bile acid dependent fashion. Using a workflow involving mouse models, clinical studies, metagenomic analyses, and mathematical modelling, we identify a probiotic candidate that corrects a clinically relevant microbiome deficiency. These findings have implications for the rational design of targeted antimicrobials as well as microbiome-based diagnostics and therapeutics for individuals at risk of C. difficile infection.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4354891/" 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/PMC4354891/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Buffie, Charlie G -- Bucci, Vanni -- Stein, Richard R -- McKenney, Peter T -- Ling, Lilan -- Gobourne, Asia -- No, Daniel -- Liu, Hui -- Kinnebrew, Melissa -- Viale, Agnes -- Littmann, Eric -- van den Brink, Marcel R M -- Jenq, Robert R -- Taur, Ying -- Sander, Chris -- Cross, Justin R -- Toussaint, Nora C -- Xavier, Joao B -- Pamer, Eric G -- AI95706/AI/NIAID NIH HHS/ -- DP2 OD008440/OD/NIH HHS/ -- DP2OD008440/OD/NIH HHS/ -- K23 AI095398/AI/NIAID NIH HHS/ -- P01 CA023766/CA/NCI NIH HHS/ -- P30 CA008748/CA/NCI NIH HHS/ -- R01 AI042135/AI/NIAID NIH HHS/ -- R01 AI095706/AI/NIAID NIH HHS/ -- R01 AI42135/AI/NIAID NIH HHS/ -- T32 CA009149/CA/NCI NIH HHS/ -- T32 GM007739/GM/NIGMS NIH HHS/ -- T32GM07739/GM/NIGMS NIH HHS/ -- U54 CA148967/CA/NCI NIH HHS/ -- England -- Nature. 2015 Jan 8;517(7533):205-8. doi: 10.1038/nature13828. Epub 2014 Oct 22.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Infectious Diseases Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [2] Lucille Castori Center for Microbes, Inflammation and Cancer, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; 1] Computational Biology Program, Sloan-Kettering Institute, New York, New York 10065, USA [2] Department of Biology, University of Massachusetts Dartmouth, North Dartmouth, Massachusetts 02747, USA. ; Computational Biology Program, Sloan-Kettering Institute, New York, New York 10065, USA. ; Lucille Castori Center for Microbes, Inflammation and Cancer, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; Donald B. and Catherine C. Marron Cancer Metabolism Center, Sloan-Kettering Institute, New York, New York 10065, USA. ; Genomics Core Laboratory, Sloan-Kettering Institute, New York, New York 10065, USA. ; 1] Bone Marrow Transplant Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [2] Immunology Program, Sloan-Kettering Institute, New York, New York 10065, USA. ; Bone Marrow Transplant Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA. ; 1] Lucille Castori Center for Microbes, Inflammation and Cancer, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [2] Computational Biology Program, Sloan-Kettering Institute, New York, New York 10065, USA. ; 1] Infectious Diseases Service, Department of Medicine, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [2] Lucille Castori Center for Microbes, Inflammation and Cancer, Memorial Sloan Kettering Cancer Center, New York, New York 10065, USA [3] Immunology Program, Sloan-Kettering Institute, New York, New York 10065, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25337874" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Bile Acids and Salts/*metabolism ; Biological Evolution ; Clostridium/metabolism ; Clostridium difficile/drug effects/*physiology ; Colitis/metabolism/microbiology/prevention & control/therapy ; Disease Susceptibility/*microbiology ; Feces/microbiology ; Female ; Humans ; Intestines/drug effects/*metabolism/*microbiology ; Metagenome/genetics ; Mice ; Mice, Inbred C57BL ; Microbiota/drug effects/genetics/*physiology ; Symbiosis
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 4
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    Calcium transient prevalence across the dendritic arbour predicts place field properties (2014)
    Nature Publishing Group (NPG)
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    Publication Date: 2014-11-05
    Description: Establishing the hippocampal cellular ensemble that represents an animal's environment involves the emergence and disappearance of place fields in specific CA1 pyramidal neurons, and the acquisition of different spatial firing properties across the active population. While such firing flexibility and diversity have been linked to spatial memory, attention and task performance, the cellular and network origin of these place cell features is unknown. Basic integrate-and-fire models of place firing propose that such features result solely from varying inputs to place cells, but recent studies suggest instead that place cells themselves may play an active role through regenerative dendritic events. However, owing to the difficulty of performing functional recordings from place cell dendrites, no direct evidence of regenerative dendritic events exists, leaving any possible connection to place coding unknown. Using multi-plane two-photon calcium imaging of CA1 place cell somata, axons and dendrites in mice navigating a virtual environment, here we show that regenerative dendritic events do exist in place cells of behaving mice, and, surprisingly, their prevalence throughout the arbour is highly spatiotemporally variable. Furthermore, we show that the prevalence of such events predicts the spatial precision and persistence or disappearance of place fields. This suggests that the dynamics of spiking throughout the dendritic arbour may play a key role in forming the hippocampal representation of space.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4289090/" 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/PMC4289090/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Sheffield, Mark E J -- Dombeck, Daniel A -- 1R01MH101297/MH/NIMH NIH HHS/ -- R01 MH101297/MH/NIMH NIH HHS/ -- England -- Nature. 2015 Jan 8;517(7533):200-4. doi: 10.1038/nature13871. Epub 2014 Oct 26.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Neurobiology, Northwestern University, Evanston, Illinois 60208, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25363782" target="_blank"〉PubMed〈/a〉
    Keywords: Action Potentials ; Animals ; Axons/metabolism ; Calcium/*metabolism ; *Calcium Signaling ; Dendrites/*metabolism ; Hippocampus/*cytology/*physiology ; Male ; Memory, Long-Term/physiology ; Mice ; Mice, Inbred C57BL ; Neuronal Plasticity/physiology ; Space Perception/*physiology ; Time Factors
    Print ISSN: 0028-0836
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 5
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    CLP1 links tRNA metabolism to progressive motor-neuron loss (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-03-12
    Description: CLP1 was the first mammalian RNA kinase to be identified. However, determining its in vivo function has been elusive. Here we generated kinase-dead Clp1 (Clp1(K/K)) mice that show a progressive loss of spinal motor neurons associated with axonal degeneration in the peripheral nerves and denervation of neuromuscular junctions, resulting in impaired motor function, muscle weakness, paralysis and fatal respiratory failure. Transgenic rescue experiments show that CLP1 functions in motor neurons. Mechanistically, loss of CLP1 activity results in accumulation of a novel set of small RNA fragments, derived from aberrant processing of tyrosine pre-transfer RNA. These tRNA fragments sensitize cells to oxidative-stress-induced p53 (also known as TRP53) activation and p53-dependent cell death. Genetic inactivation of p53 rescues Clp1(K/K) mice from the motor neuron loss, muscle denervation and respiratory failure. Our experiments uncover a mechanistic link between tRNA processing, formation of a new RNA species and progressive loss of lower motor neurons regulated by p53.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3674495/" 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/PMC3674495/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Hanada, Toshikatsu -- Weitzer, Stefan -- Mair, Barbara -- Bernreuther, Christian -- Wainger, Brian J -- Ichida, Justin -- Hanada, Reiko -- Orthofer, Michael -- Cronin, Shane J -- Komnenovic, Vukoslav -- Minis, Adi -- Sato, Fuminori -- Mimata, Hiromitsu -- Yoshimura, Akihiko -- Tamir, Ido -- Rainer, Johannes -- Kofler, Reinhard -- Yaron, Avraham -- Eggan, Kevin C -- Woolf, Clifford J -- Glatzel, Markus -- Herbst, Ruth -- Martinez, Javier -- Penninger, Josef M -- K99NS077435-01A1/NS/NINDS NIH HHS/ -- NS038253/NS/NINDS NIH HHS/ -- P 19223/Austrian Science Fund FWF/Austria -- P 21667/Austrian Science Fund FWF/Austria -- R00 NS077435/NS/NINDS NIH HHS/ -- R01 NS038253/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Mar 28;495(7442):474-80. doi: 10.1038/nature11923. Epub 2013 Mar 10.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉IMBA, Institute of Molecular Biotechnology of the Austrian Academy of Sciences, Vienna 1030, Austria.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23474986" target="_blank"〉PubMed〈/a〉
    Keywords: Amyotrophic Lateral Sclerosis ; Animals ; Animals, Newborn ; Axons/metabolism/pathology ; Cell Death ; Diaphragm/innervation ; Embryo Loss ; Embryo, Mammalian/metabolism/pathology ; Exons/genetics ; Female ; Fibroblasts ; Male ; Mice ; Mice, Inbred C57BL ; Mice, Knockout ; Mice, Transgenic ; Motor Neurons/*metabolism/*pathology ; Muscular Atrophy, Spinal ; Neuromuscular Diseases/metabolism/pathology ; Oxidative Stress ; RNA Processing, Post-Transcriptional ; RNA, Transfer, Tyr/genetics/*metabolism ; Respiration ; Spinal Nerves/cytology ; Transcription Factors/deficiency/*metabolism ; Tumor Suppressor Protein p53/metabolism ; Tyrosine/genetics/metabolism
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  • 6
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    Stabilization of cooperative virulence by the expression of an avirulent phenotype (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-02-22
    Description: Pathogens often infect hosts through collective actions: they secrete growth-promoting compounds or virulence factors, or evoke host reactions that fuel the colonization of the host. Such behaviours are vulnerable to the rise of mutants that benefit from the collective action without contributing to it; how these behaviours can be evolutionarily stable is not well understood. We address this question using the intestinal pathogen Salmonella enterica serovar Typhimurium (hereafter termed S. typhimurium), which manipulates its host to induce inflammation, and thereby outcompetes the commensal microbiota. Notably, the virulence factors needed for host manipulation are expressed in a bistable fashion, leading to a slow-growing subpopulation that expresses virulence genes, and a fast-growing subpopulation that is phenotypically avirulent. Here we show that the expression of the genetically identical but phenotypically avirulent subpopulation is essential for the evolutionary stability of virulence in this pathogen. Using a combination of mathematical modelling, experimental evolution and competition experiments we found that within-host evolution leads to the emergence of mutants that are genetically avirulent and fast-growing. These mutants are defectors that exploit inflammation without contributing to it. In infection experiments initiated with wild-type S. typhimurium, defectors increase only slowly in frequency. In a genetically modified S. typhimurium strain in which the phenotypically avirulent subpopulation is reduced in size, defectors rise more rapidly, inflammation ceases prematurely, and S. typhimurium is quickly cleared from the gut. Our results establish that host manipulation by S. typhimurium is a cooperative trait that is vulnerable to the rise of avirulent defectors; the expression of a phenotypically avirulent subpopulation that grows as fast as defectors slows down this process, and thereby promotes the evolutionary stability of virulence. This points to a key role of bistable virulence gene expression in stabilizing cooperative virulence and may lead the way to new approaches for controlling pathogens.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diard, Mederic -- Garcia, Victor -- Maier, Lisa -- Remus-Emsermann, Mitja N P -- Regoes, Roland R -- Ackermann, Martin -- Hardt, Wolf-Dietrich -- England -- Nature. 2013 Feb 21;494(7437):353-6. doi: 10.1038/nature11913.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Institute of Microbiology, ETH Zurich, Wolfgang-Pauli-Str. 10, 8093 Zurich, Switzerland.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23426324" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; *Biological Evolution ; Host-Pathogen Interactions ; Inflammation/microbiology/pathology ; Intestines/microbiology ; Mice ; Mice, Inbred C57BL ; Mutation ; *Phenotype ; Salmonella Infections/microbiology/prevention & control/transmission ; Salmonella typhimurium/genetics/growth & development/*pathogenicity ; Virulence/genetics/physiology ; Virulence Factors/genetics/metabolism
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  • 7
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    Microbiota restricts trafficking of bacteria to mesenteric lymph nodes by CX(3)CR1(hi) cells (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-01-22
    Description: The intestinal microbiota has a critical role in immune system and metabolic homeostasis, but it must be tolerated by the host to avoid inflammatory responses that can damage the epithelial barrier separating the host from the luminal contents. Breakdown of this regulation and the resulting inappropriate immune response to commensals are thought to lead to the development of inflammatory bowel diseases such as Crohn's disease and ulcerative colitis. We proposed that the intestinal immune system is instructed by the microbiota to limit responses to luminal antigens. Here we demonstrate in mice that, at steady state, the microbiota inhibits the transport of both commensal and pathogenic bacteria from the lumen to a key immune inductive site, the mesenteric lymph nodes (MLNs). However, in the absence of Myd88 or under conditions of antibiotic-induced dysbiosis, non-invasive bacteria were trafficked to the MLNs in a CCR7-dependent manner, and induced both T-cell responses and IgA production. Trafficking was carried out by CX(3)CR1(hi) mononuclear phagocytes, an intestinal-cell population previously reported to be non-migratory. These findings define a central role for commensals in regulating the migration to the MLNs of CX(3)CR1(hi) mononuclear phagocytes endowed with the ability to capture luminal bacteria, thereby compartmentalizing the intestinal immune response to avoid inflammation.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3711636/" 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/PMC3711636/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Diehl, Gretchen E -- Longman, Randy S -- Zhang, Jing-Xin -- Breart, Beatrice -- Galan, Carolina -- Cuesta, Adolfo -- Schwab, Susan R -- Littman, Dan R -- 5P30CA016087-32/CA/NCI NIH HHS/ -- R01 AI085166/AI/NIAID NIH HHS/ -- R01AI085166/AI/NIAID NIH HHS/ -- T32 CA009161/CA/NCI NIH HHS/ -- T32 DK083256/DK/NIDDK NIH HHS/ -- T32 DK083256-02/DK/NIDDK NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Feb 7;494(7435):116-20. doi: 10.1038/nature11809. Epub 2013 Jan 13.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Molecular Pathogenesis Program, The Kimmel Center for Biology and Medicine of the Skirball Institute, New York University School of Medicine, New York, New York 10016, USA. Gretchen.Diehl@med.nyu.edu〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23334413" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Anti-Bacterial Agents/pharmacology ; Antigens, Bacterial/immunology ; Cell Movement ; Dendritic Cells/cytology/immunology ; Immunity, Mucosal/drug effects/*immunology ; Immunoglobulin A/immunology ; Inflammation/immunology ; Intestinal Mucosa/cytology/immunology/microbiology ; Lymph Nodes/*immunology/*microbiology ; Mesentery/*immunology ; Metagenome/immunology/*physiology ; Mice ; Mice, Inbred C57BL ; Myeloid Differentiation Factor 88/deficiency/metabolism ; Phagocytes/cytology/immunology/*metabolism/microbiology ; Phagocytosis ; Receptors, CCR7/deficiency/genetics/metabolism ; Receptors, Chemokine/*metabolism ; Salmonella/cytology/drug effects/immunology ; T-Lymphocytes/immunology
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    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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  • 8
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    Arteriolar niches maintain haematopoietic stem cell quiescence (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-10-11
    Description: Cell cycle quiescence is a critical feature contributing to haematopoietic stem cell (HSC) maintenance. Although various candidate stromal cells have been identified as potential HSC niches, the spatial localization of quiescent HSCs in the bone marrow remains unclear. Here, using a novel approach that combines whole-mount confocal immunofluorescence imaging techniques and computational modelling to analyse significant three-dimensional associations in the mouse bone marrow among vascular structures, stromal cells and HSCs, we show that quiescent HSCs associate specifically with small arterioles that are preferentially found in endosteal bone marrow. These arterioles are ensheathed exclusively by rare NG2 (also known as CSPG4)(+) pericytes, distinct from sinusoid-associated leptin receptor (LEPR)(+) cells. Pharmacological or genetic activation of the HSC cell cycle alters the distribution of HSCs from NG2(+) periarteriolar niches to LEPR(+) perisinusoidal niches. Conditional depletion of NG2(+) cells induces HSC cycling and reduces functional long-term repopulating HSCs in the bone marrow. These results thus indicate that arteriolar niches are indispensable for maintaining HSC quiescence.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3821873/" 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/PMC3821873/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Kunisaki, Yuya -- Bruns, Ingmar -- Scheiermann, Christoph -- Ahmed, Jalal -- Pinho, Sandra -- Zhang, Dachuan -- Mizoguchi, Toshihide -- Wei, Qiaozhi -- Lucas, Daniel -- Ito, Keisuke -- Mar, Jessica C -- Bergman, Aviv -- Frenette, Paul S -- HL069438/HL/NHLBI NIH HHS/ -- HL097700/HL/NHLBI NIH HHS/ -- R00 CA139009/CA/NCI NIH HHS/ -- R01 DK056638/DK/NIDDK NIH HHS/ -- R01 DK098263/DK/NIDDK NIH HHS/ -- R01 DK100689/DK/NIDDK NIH HHS/ -- R01 HL069438/HL/NHLBI NIH HHS/ -- R01 HL097700/HL/NHLBI NIH HHS/ -- R01 HL116340/HL/NHLBI NIH HHS/ -- T32 063754/PHS HHS/ -- England -- Nature. 2013 Oct 31;502(7473):637-43. doi: 10.1038/nature12612. Epub 2013 Oct 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉1] Ruth L. and David S. Gottesman Institute for Stem Cell and Regenerative Medicine Research, Albert Einstein College of Medicine, Bronx, New York 10461, USA [2] Department of Cell Biology, Albert Einstein College of Medicine, Bronx, New York 10461, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24107994" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Arterioles/*cytology ; Bone Marrow/blood supply ; Cell Division ; Cell Separation ; Female ; Flow Cytometry ; Hematopoietic Stem Cells/*cytology/metabolism ; Male ; Mesenchymal Stromal Cells/cytology ; Mice ; Mice, Inbred C57BL ; Nestin/metabolism ; *Stem Cell Niche
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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    Proteolytic elimination of N-myristoyl modifications by the Shigella virulence factor IpaJ (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-03-29
    Description: Protein N-myristoylation is a 14-carbon fatty-acid modification that is conserved across eukaryotic species and occurs on nearly 1% of the cellular proteome. The ability of the myristoyl group to facilitate dynamic protein-protein and protein-membrane interactions (known as the myristoyl switch) makes it an essential feature of many signal transduction systems. Thus pathogenic strategies that facilitate protein demyristoylation would markedly alter the signalling landscape of infected host cells. Here we describe an irreversible mechanism of protein demyristoylation catalysed by invasion plasmid antigen J (IpaJ), a previously uncharacterized Shigella flexneri type III effector protein with cysteine protease activity. A yeast genetic screen for IpaJ substrates identified ADP-ribosylation factor (ARF)1p and ARF2p, small molecular mass GTPases that regulate cargo transport through the Golgi apparatus. Mass spectrometry showed that IpaJ cleaved the peptide bond between N-myristoylated glycine-2 and asparagine-3 of human ARF1, thereby providing a new mechanism for host secretory inhibition by a bacterial pathogen. We further demonstrate that IpaJ cleaves an array of N-myristoylated proteins involved in cellular growth, signal transduction, autophagasome maturation and organelle function. Taken together, these findings show a previously unrecognized pathogenic mechanism for the site-specific elimination of N-myristoyl protein modification.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3722872/" 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/PMC3722872/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Burnaevskiy, Nikolay -- Fox, Thomas G -- Plymire, Daniel A -- Ertelt, James M -- Weigele, Bethany A -- Selyunin, Andrey S -- Way, Sing Sing -- Patrie, Steven M -- Alto, Neal M -- 5T32AI007520/AI/NIAID NIH HHS/ -- R01 AI083359/AI/NIAID NIH HHS/ -- R01 AI087830/AI/NIAID NIH HHS/ -- R01 AI100934/AI/NIAID NIH HHS/ -- R01 GM100486/GM/NIGMS NIH HHS/ -- R01AI083359/AI/NIAID NIH HHS/ -- R01GM100486/GM/NIGMS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Apr 4;496(7443):106-9. doi: 10.1038/nature12004. Epub 2013 Mar 27.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Microbiology, University of Texas Southwestern Medical Center, 5323 Harry Hines Boulevard, Dallas, Texas 75390-8816, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23535599" target="_blank"〉PubMed〈/a〉
    Keywords: ADP-Ribosylation Factor 1/chemistry/metabolism ; ADP-Ribosylation Factors/metabolism ; Amino Acid Sequence ; Animals ; Antigens, Bacterial/*metabolism ; Asparagine/metabolism ; Autophagy ; Biocatalysis ; Cysteine Proteases/metabolism ; Dysentery, Bacillary ; Female ; Glycine/metabolism ; Golgi Apparatus/metabolism/pathology ; HEK293 Cells ; HeLa Cells ; Humans ; Listeria monocytogenes/physiology ; Mice ; Mice, Inbred C57BL ; Molecular Sequence Data ; Myristic Acid/*metabolism ; Phagosomes/metabolism ; *Protein Processing, Post-Translational ; *Proteolysis ; Saccharomyces cerevisiae ; Saccharomyces cerevisiae Proteins/metabolism ; Sequence Alignment ; Shigella flexneri/enzymology/*metabolism ; Signal Transduction ; Substrate Specificity ; Virulence ; Virulence Factors/*metabolism
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
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    Reprogramming in vivo produces teratomas and iPS cells with totipotency features (2013)
    Nature Publishing Group (NPG)
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    Publication Date: 2013-09-13
    Description: Reprogramming of adult cells to generate induced pluripotent stem cells (iPS cells) has opened new therapeutic opportunities; however, little is known about the possibility of in vivo reprogramming within tissues. Here we show that transitory induction of the four factors Oct4, Sox2, Klf4 and c-Myc in mice results in teratomas emerging from multiple organs, implying that full reprogramming can occur in vivo. Analyses of the stomach, intestine, pancreas and kidney reveal groups of dedifferentiated cells that express the pluripotency marker NANOG, indicative of in situ reprogramming. By bone marrow transplantation, we demonstrate that haematopoietic cells can also be reprogrammed in vivo. Notably, reprogrammable mice present circulating iPS cells in the blood and, at the transcriptome level, these in vivo generated iPS cells are closer to embryonic stem cells (ES cells) than standard in vitro generated iPS cells. Moreover, in vivo iPS cells efficiently contribute to the trophectoderm lineage, suggesting that they achieve a more plastic or primitive state than ES cells. Finally, intraperitoneal injection of in vivo iPS cells generates embryo-like structures that express embryonic and extraembryonic markers. We conclude that reprogramming in vivo is feasible and confers totipotency features absent in standard iPS or ES cells. These discoveries could be relevant for future applications of reprogramming in regenerative medicine.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Abad, Maria -- Mosteiro, Lluc -- Pantoja, Cristina -- Canamero, Marta -- Rayon, Teresa -- Ors, Inmaculada -- Grana, Osvaldo -- Megias, Diego -- Dominguez, Orlando -- Martinez, Dolores -- Manzanares, Miguel -- Ortega, Sagrario -- Serrano, Manuel -- England -- Nature. 2013 Oct 17;502(7471):340-5. doi: 10.1038/nature12586. Epub 2013 Sep 11.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Tumour Suppression Group, Spanish National Cancer Research Centre (CNIO), Madrid E-28029, Spain.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24025773" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Blood Cells/cytology/metabolism ; Cell Dedifferentiation ; Cell Separation ; Cells, Cultured ; *Cellular Reprogramming/genetics ; Ectoderm/cytology ; Embryoid Bodies/cytology/metabolism ; Embryonic Stem Cells/cytology/metabolism ; Female ; Fibroblasts/cytology ; Gene Expression Profiling ; Induced Pluripotent Stem Cells/*cytology/metabolism ; Intestines/cytology ; Kidney/cytology ; Kruppel-Like Transcription Factors/genetics/metabolism ; Male ; Mice ; Mice, Inbred C57BL ; Octamer Transcription Factor-3/genetics/metabolism ; Organ Specificity ; Pancreas/cytology ; Proto-Oncogene Proteins c-myc/genetics/metabolism ; SOXB1 Transcription Factors/genetics/metabolism ; Stomach/cytology ; Teratoma/genetics/*metabolism/pathology ; Totipotent Stem Cells/*cytology/metabolism ; Transcriptome/genetics ; Trophoblasts/cytology
    Print ISSN: 0028-0836
    Electronic ISSN: 1476-4687
    Topics: Biology , Chemistry and Pharmacology , Medicine , Natural Sciences in General , Physics
    Published by Nature Publishing Group (NPG)
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