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|a Kim, Dennis H.
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|a Massachusetts Institute of Technology. Department of Biology
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|a Kim, Dennis H.
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|a Kim, Dennis H.
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|a Pagano, Daniel Joseph
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|a Kooistra, Tristan G.
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|a Chu, Stephanie W.
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|a Shivers, Robert P.
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|a Pagano, Daniel Joseph
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|a Kooistra, Tristan G.
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|a Chu, Stephanie W.
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|a Shivers, Robert P.
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|a Tissue-Specific Activities of SARM-ASK1-MKK3 Signaling Coordinate Immunity and Behavior to Pathogenic and Nutritional Bacteria in C. elegans
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|a Tissue-Specific Activities of an Immune Signaling Module Regulate Physiological Responses to Pathogenic and Nutritional Bacteria in C. elegans
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|b Cell Press,
|c 2010-07-15T15:52:30Z.
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|z Get fulltext
|u http://hdl.handle.net/1721.1/56561
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|a Microbes represent both an essential source of nutrition and a potential source of lethal infection to the nematode Caenorhabditis elegans. Immunity in C. elegans requires a signaling module comprised of orthologs of the mammalian Toll-interleukin-1 receptor (TIR) domain protein SARM, the mitogen-activated protein kinase kinase kinase (MAPKKK) ASK1, and MAPKK MKK3, which activates p38 MAPK. We determined that the SARM-ASK1-MKK3 module has dual tissue-specific roles in the C. elegans response to pathogens-in the cell-autonomous regulation of innate immunity and the neuroendocrine regulation of serotonin-dependent aversive behavior. SARM-ASK1-MKK3 signaling in the sensory nervous system also regulates egg-laying behavior that is dependent on bacteria provided as a nutrient source. Our data demonstrate that these physiological responses to bacteria share a common mechanism of signaling through the SARM-ASK1-MKK3 module and suggest the co-option of ancestral immune signaling pathways in the evolution of physiological responses to microbial pathogens and nutrients.
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|a United States National Institutes of Health (GM084477)
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|a Burroughs Wellcome Fund
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|a en_US
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|a Microbio
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|a Molimmuno
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|a Article
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|t Cell Host and Microbe
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