daf-28encodes aC. elegansinsulin superfamily member that is regulated by environmental cues and acts in the DAF-2 signaling pathway
Open Access
- 21 March 2003
- journal article
- research article
- Published by Cold Spring Harbor Laboratory in Genes & Development
- Vol. 17 (7), 844-858
- https://doi.org/10.1101/gad.1066503
Abstract
In Caenorhabditis elegans, the decision to enter a developmentally arrested dauer larval stage is triggered by a combination of signals from sensory neurons in response to environmental cues, which include a dauer pheromone. These sensory inputs are coupled to the parallel DAF-2/insulin receptor-like and DAF-7/TGFβ-like signaling pathways. Although sensory inputs have been shown to physiologically regulate DAF-7/TGFβ expression, no such regulation of insulin-like ligands in the DAF-2 pathway has been reported. We show here that daf-28 encodes an insulin-like protein, which when mutated causes dauer arrest and down-regulation of DAF-2/IR signaling. A daf-28∷GFP fusion gene is expressed in ASI and ASJ, two sensory neurons that regulate dauer arrest.daf-28∷GFP expression in ASI and ASJ is down-regulated under dauer-inducing conditions and in mutants of DAF-11/guanylyl cyclase, a predicted component of the dauer-pheromone-sensing pathway. Thus,daf-28 expression in sensory neurons is regulated by the environmental cues that normally trigger dauer arrest. Among the 38C. elegans insulin genes, daf-28 is so far the only insulin mutant to affect dauer arrest. daf-28 was revealed from this functional redundancy by a dominant-negative allele that disrupts a probable proteolytic processing site required for insulin maturation. This DAF-28 mutant is likely to be poisonous to wild-type DAF-28 and other insulins.Keywords
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