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  • 1
    Publication Date: 2010-10-12
    Description: Population density-dependent dispersal is a well-characterized strategy of animal behavior in which dispersal rate increases when population density is higher. Caenorhabditis elegans shows positive chemotaxis to a set of odorants, but the chemotaxis switches from attraction to dispersal after prolonged exposure to the odorants. We show here that this plasticity of olfactory behavior is dependent on population density and that this regulation is mediated by pheromonal signaling. We show that a peptide, suppressor of NEP-2 (SNET-1), negatively regulates olfactory plasticity and that its expression is down-regulated by the pheromone. NEP-2, a homolog of the extracellular peptidase neprilysin, antagonizes SNET-1, and this function is essential for olfactory plasticity. These results suggest that population density information is transmitted through the external pheromone and endogenous peptide signaling to modulate chemotactic behavior.〈br /〉〈br /〉〈a href="https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3021133/" 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/PMC3021133/" target="_blank"〉This paper as free author manuscript - peer-reviewed and accepted for publication〈/a〉〈br /〉〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Yamada, Koji -- Hirotsu, Takaaki -- Matsuki, Masahiro -- Butcher, Rebecca A -- Tomioka, Masahiro -- Ishihara, Takeshi -- Clardy, Jon -- Kunitomo, Hirofumi -- Iino, Yuichi -- CA24487/CA/NCI NIH HHS/ -- GM087533/GM/NIGMS NIH HHS/ -- K99 GM087533/GM/NIGMS NIH HHS/ -- K99 GM087533-01/GM/NIGMS NIH HHS/ -- R00 GM087533/GM/NIGMS NIH HHS/ -- R00 GM087533-03/GM/NIGMS NIH HHS/ -- New York, N.Y. -- Science. 2010 Sep 24;329(5999):1647-50. doi: 10.1126/science.1192020.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biophysics and Biochemistry, Graduate School of Science, University of Tokyo, Tokyo 113-0032, Japan.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/20929849" target="_blank"〉PubMed〈/a〉
    Keywords: *Adaptation, Physiological ; Animals ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/*metabolism ; *Chemotaxis ; Down-Regulation ; Gene Expression Regulation ; Mutation ; Neprilysin/genetics/*metabolism ; Neurites/metabolism ; Neurons/metabolism ; Odors ; Olfactory Pathways/cytology/physiology ; Pheromones/*metabolism ; Population Density ; Recombinant Fusion Proteins/metabolism ; Repressor Proteins/genetics/*metabolism ; *Signal Transduction ; Smell/physiology
    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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  • 2
    Publication Date: 2014-07-19
    Description: The phosphatidylinositol 3-kinase (PI3K) pathway regulates many cellular functions, but its roles in the nervous system are still poorly understood. We found that a newly discovered insulin receptor isoform, DAF-2c, is translocated from the cell body to the synaptic region of the chemosensory neuron in Caenorhabditis elegans by a conditioning stimulus that induces taste avoidance learning. This translocation is essential for learning and is dependent on the mitogen-activated protein kinase-regulated interaction of CASY-1 (the calsyntenin ortholog) and kinesin-1. The PI3K pathway is required downstream of the receptor. Light-regulated activation of PI3K in the synaptic region, but not in other parts of the cell, switched taste-attractive behavior to taste avoidance, mimicking the effect of conditioning. Thus, synaptic PI3K is crucial for the behavioral switch caused by learning.〈br /〉〈span class="detail_caption"〉Notes: 〈/span〉Ohno, Hayao -- Kato, Shinya -- Naito, Yasuki -- Kunitomo, Hirofumi -- Tomioka, Masahiro -- Iino, Yuichi -- New York, N.Y. -- Science. 2014 Jul 18;345(6194):313-7. doi: 10.1126/science.1250709.〈br /〉〈span class="detail_caption"〉Author address: 〈/span〉Department of Biological Sciences, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan. JST, CREST, 4-1-8 Honcho, Kawaguchi, Saitama 332-0012, Japan. ; Department of Biological Sciences, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan. ; Department of Biological Sciences, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan. Molecular Genetics Research Laboratory, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan. ; Molecular Genetics Research Laboratory, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan. seidai@gen.s.u-tokyo.ac.jp iino@bs.s.u-tokyo.ac.jp. ; Department of Biological Sciences, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan. JST, CREST, 4-1-8 Honcho, Kawaguchi, Saitama 332-0012, Japan. Molecular Genetics Research Laboratory, Graduate School of Science, University of Tokyo, Tokyo 113-0033, Japan. seidai@gen.s.u-tokyo.ac.jp iino@bs.s.u-tokyo.ac.jp.〈br /〉〈span class="detail_caption"〉Record origin:〈/span〉 〈a href="http://www.ncbi.nlm.nih.gov/pubmed/25035490" target="_blank"〉PubMed〈/a〉
    Keywords: Animals ; Behavior, Animal/*physiology ; Caenorhabditis elegans/genetics/*physiology ; Caenorhabditis elegans Proteins/genetics/metabolism/*physiology ; Learning/*physiology ; Light ; Phosphatidylinositol 3-Kinases/genetics/*physiology ; Protein Isoforms/metabolism ; Receptor, Insulin/metabolism ; Synapses/*enzymology
    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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