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- W2980708595 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 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." @default.
- W2980708595 created "2019-10-25" @default.
- W2980708595 creator A5026214120 @default.
- W2980708595 creator A5046966290 @default.
- W2980708595 creator A5069591604 @default.
- W2980708595 date "2019-01-01" @default.
- W2980708595 modified "2023-10-02" @default.
- W2980708595 title "Repression of an activity-dependent autocrine insulin signal is required for sensory neuron development in<i>C. elegans</i>" @default.
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- W2980708595 doi "https://doi.org/10.1242/dev.182873" @default.
- W2980708595 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/6899041" @default.
- W2980708595 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/31628111" @default.
- W2980708595 hasPublicationYear "2019" @default.
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