title: Endogenous RNAi Pathways Are Required in Neurons for Dauer Formation inCaenorhabditis elegans.
abstract: Animals can adapt to unfavorable environments through changes in physiology or behavior. In the nematode,Caenorhabditis elegans, environmental conditions perceived early in development determine whether the animal enters either the reproductive cycle, or enters into an alternative diapause stage named dauer. Here, we show that endogenous RNAi pathways play a role in dauer formation in crowding (high pheromone), starvation, and high temperature conditions. Disruption of theMutatorproteins or the nuclear Argonaute CSR-1 result in differential dauer-deficient phenotypes that are dependent upon the experienced environmental stress. We provide evidence that the RNAi pathways function in chemosensory neurons for dauer formation, upstream of the TGF-β and insulin signaling pathways. In addition, we show thatMutatorMUT-16 expression in a subset of individual pheromone-sensing neurons is sufficient for dauer formation in high pheromone conditions, but not in starvation or high temperature conditions. Furthermore, we also show that MUT-16 and CSR-1 are required for expression of a subset of G proteins with functions in the detection of pheromone components. Together, our data suggest a model whereMutator-amplified siRNAs that associate with the CSR-1 pathway promote expression of genes required for the detection and signaling of environmental conditions to regulate development and behavior inC. elegansThis study highlights a mechanism whereby RNAi pathways mediate the link between environmental stress and adaptive phenotypic plasticity in animals.
authors.affiliation: Department of Biology, Syracuse University, New York 13244.
authors.forename: Pallavi S
authors.initials: PS
authors.lastname: Bharadwaj
authors.affiliation: Department of Biology, Syracuse University, New York 13244 shall@syr.edu.
authors.forename: Sarah E
authors.identifier: 0000-0002-8536-4000
authors.initials: SE
authors.lastname: Hall
mesh_terms: D000818:Animals; D017173:Caenorhabditis elegans / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism; D029742:Caenorhabditis elegans Proteins / Q000235:genetics / Q000378:metabolism; D019204:GTP-Binding Proteins / Q000235:genetics / Q000378:metabolism; D018507:Gene Expression Regulation, Developmental; D007328:Insulin / Q000378:metabolism; D010675:Pheromones / Q000378:metabolism; D034622:RNA Interference; D011984:Sensory Receptor Cells / Q000378:metabolism*; D015398:Signal Transduction; D016212:Transforming Growth Factor beta / Q000378:metabolism
chemical_list: C544459:CSR-1 protein, C elegans; D029742:Caenorhabditis elegans Proteins; D007328:Insulin; C557694:MUT-16 protein, C elegans; D010675:Pheromones; D016212:Transforming Growth Factor beta; D019204:GTP-Binding Proteins
keywords: CSR-1; Caenorhabditis elegans; Mutators; RNAi; dauer