DOI: 10.1101/481010Nov 28, 2018Paper

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

BioRxiv : the Preprint Server for Biology
Lauren Bayer HorowitzNiels Ringstad

Abstract

Nervous system development is instructed both by genetic programs and activity-dependent refinement of gene expression and connectivity. How these mechanisms 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, functions by limiting expression of an autocrine ILP signal that represses a chemosensory-neuron fate. ILPs are released from BAGs in an activity-dependent manner during embryonic development, and regulate neurodifferentiation through a non-canonical insulin receptor signaling pathway. The differentiation of a specialized neuron-type is, therefore, coordinately regulated by a genetic program that controls ILP expression and by neural activity, which regulates ILP release. Autocrine signals of this kind may have general and conserved functions as integrators of deterministic genetic programs with activity-dependent mechanisms during neurodevelopment.

Related Concepts

Cell Differentiation Process
Embryonic Development
Enzyme Repression
Gene Expression
Insulin
Neuroma
Neurons
Afferent Neuron
Insulin Receptor
Signal Pathways

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