Repression of an activity-dependent autocrine insulin signal is required for sensory neuron development in C. elegans.

ABSTRACT: Nervous system development is instructed by genetic programs and refined by distinct mechanisms that couple neural activity to gene expression. How these processes are integrated remains poorly understood. Here, we report that the regulated release of insulin-like peptides (ILPs) during development of the Caenorhabditis elegans nervous system accomplishes such an integration. We find that the p38 MAP kinase PMK-3, which is required for the differentiation of chemosensory BAG neurons, limits an ILP signal that represses expression of a BAG neuron fate. ILPs are released from BAGs themselves in an activity-dependent manner during development, indicating that ILPs constitute an autocrine signal that regulates the differentiation of BAG neurons. Expression of a specialized neuronal fate

SUBMITTER: Horowitz LB 

PROVIDER: S-EPMC6899041 | biostudies-literature | 2019 Nov

REPOSITORIES: biostudies-literature