Conserved autism-associated genes tune social feeding behavior in C. elegans

Mara H. Cowen, Dustin Haskell, Kristi Zoga, Kirthi C. Reddy, Sreekanth H. Chalasani and Michael P. Hart ()
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Mara H. Cowen: University of Pennsylvania
Dustin Haskell: University of Pennsylvania
Kristi Zoga: University of Pennsylvania
Kirthi C. Reddy: Salk Institute
Sreekanth H. Chalasani: Salk Institute
Michael P. Hart: University of Pennsylvania

Nature Communications, 2024, vol. 15, issue 1, 1-15

Abstract: Abstract Animal foraging is an essential and evolutionarily conserved behavior that occurs in social and solitary contexts, but the underlying molecular pathways are not well defined. We discover that conserved autism-associated genes (NRXN1(nrx-1), NLGN3(nlg-1), GRIA1,2,3(glr-1), GRIA2(glr-2), and GLRA2,GABRA3(avr-15)) regulate aggregate feeding in C. elegans, a simple social behavior. NRX-1 functions in chemosensory neurons (ADL and ASH) independently of its postsynaptic partner NLG-1 to regulate social feeding. Glutamate from these neurons is also crucial for aggregate feeding, acting independently of NRX-1 and NLG-1. Compared to solitary counterparts, social animals show faster presynaptic release and more presynaptic release sites in ASH neurons, with only the latter requiring nrx-1. Disruption of these distinct signaling components additively converts behavior from social to solitary. Collectively, we find that aggregate feeding is tuned by conserved autism-associated genes through complementary synaptic mechanisms, revealing molecular principles driving social feeding.

Date: 2024
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DOI: 10.1038/s41467-024-53590-x

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