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  • 1
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    Drosophila NOMPC is a mechanotransduction channel subunit for gentle-touch sensation (2012)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2012-12-12
    Description: Touch sensation is essential for behaviours ranging from environmental exploration to social interaction; however, the underlying mechanisms are largely unknown. In Drosophila larvae, two types of sensory neurons, class III and class IV dendritic arborization neurons, tile the body wall. The mechanotransduction channel PIEZO in class IV neurons is essential for sensing noxious mechanical stimuli but is not involved in gentle touch. On the basis of electrophysiological-recording, calcium-imaging and behavioural studies, here we report that class III dendritic arborization neurons are touch sensitive and contribute to gentle-touch sensation. We further identify NOMPC (No mechanoreceptor potential C), a member of the transient receptor potential (TRP) family of ion channels, as a mechanotransduction channel for gentle touch. NOMPC is highly expressed in class III neurons and is required for their mechanotransduction. Moreover, ectopic NOMPC expression confers touch sensitivity to the normally touch-insensitive class IV neurons. In addition to the critical role of NOMPC in eliciting gentle-touch-mediated behavioural responses, expression of this protein in the Drosophila S2 cell line also gives rise to mechanosensitive channels in which ion selectivity can be altered by NOMPC mutation, indicating that NOMPC is a pore-forming subunit of a mechanotransduction channel. Our study establishes NOMPC as a bona fide mechanotransduction channel that satisfies all four criteria proposed for a channel to qualify as a transducer of mechanical stimuli and mediates gentle-touch sensation. Our study also suggests that different mechanosensitive channels may be used to sense gentle touch versus noxious mechanical stimuli.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3917554/" 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/PMC3917554/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yan, Zhiqiang -- Zhang, Wei -- He, Ye -- Gorczyca, David -- Xiang, Yang -- Cheng, Li E -- Meltzer, Shan -- Jan, Lily Yeh -- Jan, Yuh Nung -- 5R01MH084234/MH/NIMH NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- R01 MH084234/MH/NIMH NIH HHS/ -- R37 NS040929/NS/NINDS NIH HHS/ -- R37NS040929/NS/NINDS NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Jan 10;493(7431):221-5. doi: 10.1038/nature11685. Epub 2012 Dec 9.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Howard Hughes Medical Institute, Department of Physiology, University of California, San Francisco, San Francisco, California 94158, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/23222543" target="_blank"〉PubMed〈/a〉
    Keywords: Amino Acid Sequence ; Animals ; Cell Line ; Dendrites/physiology ; Drosophila Proteins/chemistry/genetics/*metabolism ; Drosophila melanogaster/cytology/growth & development/*physiology ; Larva/cytology/physiology ; Mechanotransduction, Cellular/*physiology ; Molecular Sequence Data ; Mutation ; Protein Subunits/chemistry/genetics/*metabolism ; Sequence Alignment ; Touch/*physiology ; Transient Receptor Potential Channels/chemistry/genetics/*metabolism
    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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  • 2
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    Type 2 innate lymphoid cells control eosinophil homeostasis (2013)
    Nature Publishing Group (NPG)
    Details
    Publication Date: 2013-09-17
    Description: Eosinophils are specialized myeloid cells associated with allergy and helminth infections. Blood eosinophils demonstrate circadian cycling, as described over 80 years ago, and are abundant in the healthy gastrointestinal tract. Although a cytokine, interleukin (IL)-5, and chemokines such as eotaxins mediate eosinophil development and survival, and tissue recruitment, respectively, the processes underlying the basal regulation of these signals remain unknown. Here we show that serum IL-5 levels are maintained by long-lived type 2 innate lymphoid cells (ILC2) resident in peripheral tissues. ILC2 cells secrete IL-5 constitutively and are induced to co-express IL-13 during type 2 inflammation, resulting in localized eotaxin production and eosinophil accumulation. In the small intestine where eosinophils and eotaxin are constitutive, ILC2 cells co-express IL-5 and IL-13; this co-expression is enhanced after caloric intake. The circadian synchronizer vasoactive intestinal peptide also stimulates ILC2 cells through the VPAC2 receptor to release IL-5, linking eosinophil levels with metabolic cycling. Tissue ILC2 cells regulate basal eosinophilopoiesis and tissue eosinophil accumulation through constitutive and stimulated cytokine expression, and this dissociated regulation can be tuned by nutrient intake and central circadian rhythms.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3795960/" 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/PMC3795960/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Nussbaum, Jesse C -- Van Dyken, Steven J -- von Moltke, Jakob -- Cheng, Laurence E -- Mohapatra, Alexander -- Molofsky, Ari B -- Thornton, Emily E -- Krummel, Matthew F -- Chawla, Ajay -- Liang, Hong-Erh -- Locksley, Richard M -- AI007334/AI/NIAID NIH HHS/ -- AI007641/AI/NIAID NIH HHS/ -- AI026918/AI/NIAID NIH HHS/ -- AI030663/AI/NIAID NIH HHS/ -- AI078869/AI/NIAID NIH HHS/ -- DK063720/DK/NIDDK NIH HHS/ -- DP1 AR064158/AR/NIAMS NIH HHS/ -- HL107202/HL/NHLBI NIH HHS/ -- P01 HL024136/HL/NHLBI NIH HHS/ -- P01 HL107202/HL/NHLBI NIH HHS/ -- P30 DK063720/DK/NIDDK NIH HHS/ -- R01 AI030663/AI/NIAID NIH HHS/ -- R37 AI026918/AI/NIAID NIH HHS/ -- T32 AI007641/AI/NIAID NIH HHS/ -- T32 GM007618/GM/NIGMS NIH HHS/ -- T32 HD044331/HD/NICHD NIH HHS/ -- U19 AI077439/AI/NIAID NIH HHS/ -- Howard Hughes Medical Institute/ -- England -- Nature. 2013 Oct 10;502(7470):245-8. doi: 10.1038/nature12526. Epub 2013 Sep 15.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Medicine, University of California San Francisco, San Francisco, California 94143-0795, USA.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/24037376" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Cells, Cultured ; Circadian Rhythm ; Collagen/metabolism ; Eosinophils/immunology/*metabolism/parasitology ; Female ; Gene Expression Regulation ; *Homeostasis ; Interleukin-13/genetics/metabolism ; Interleukin-5/blood/genetics/metabolism ; Lung/immunology/metabolism/parasitology ; Lymphocytes/immunology/*metabolism/parasitology ; Male ; Mice ; Mice, Inbred C57BL ; Nippostrongylus/physiology ; Strongylida Infections/immunology
    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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  • 3
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    Enhanced signaling through the IL-2 receptor in CD8+ T cells regulated by antigen recognition results in preferential proliferation and expansion of responding CD8+ T cells rather than promotion of cell death (2002)
    National Academy of Sciences
    Details
    Publication Date: 2002-02-26
    Print ISSN: 0027-8424
    Electronic ISSN: 1091-6490
    Topics: Biology , Medicine , Natural Sciences in General
    Published by National Academy of Sciences
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  • 4
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    Functional redundancy of the Nur77 and Nor-1 orphan steroid receptors in T-cell apoptosis (1997)
    EMBO Press
    Details
    Publication Date: 1997-04-15
    Print ISSN: 0261-4189
    Electronic ISSN: 1460-2075
    Topics: Biology , Medicine
    Published by EMBO Press on behalf of European Molecular Biology Organization.
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