Open AccessRepression of an activity-dependent autocrine insulin signal is required for sensory neuron development inC. elegans
Author(s) -
Lauren Bayer Horowitz,
Julia P. Brandt,
Niels Ringstad
Publication year - 2019
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.754
H-Index - 325
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.182873
Subject(s) - biology , autocrine signalling , caenorhabditis elegans , neuroscience , psychological repression , nervous system , signal transduction , microbiology and biotechnology , sensory neuron , neural development , cell fate determination , sensory system , neuron , regulation of gene expression , gene , gene expression , genetics , transcription factor , receptor
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 C. 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.