RRC ID 59510
Author Horowitz LB, Brandt JP, Ringstad N.
Title Repression of an activity-dependent autocrine insulin signal is required for sensory neuron development in C. elegans.
Journal Development
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 is, therefore, coordinately regulated by a genetic program that sets levels of ILP expression during development, and by neural activity, which regulates ILP release. Autocrine signals of this kind might have general and conserved functions as integrators of deterministic genetic programs with activity-dependent mechanisms during neurodevelopment.
Volume 146(22)
Published 2019-11-19
DOI 10.1242/dev.182873
PII dev.182873
PMID 31628111
PMC PMC6899041
MeSH Alleles Animals Autocrine Communication Caenorhabditis elegans / embryology* Caenorhabditis elegans Proteins / metabolism* Calcium / metabolism Cell Lineage Gene Expression Regulation, Developmental* Genotype Green Fluorescent Proteins / metabolism Heat-Shock Proteins / metabolism Insulin / metabolism* Mitogen-Activated Protein Kinases / metabolism* Mutation Nervous System / embryology* Peptides / chemistry RNA-Seq Sensory Receptor Cells / metabolism* Signal Transduction Transgenes
IF 5.763
Times Cited 0
C.elegans tm1734 tm2816 tm2308