Conserved autism-associated genes tune social feeding behavior in C. elegans
Mara H. Cowen, Dustin Haskell, Kristi Zoga, Kirthi C. Reddy, Sreekanth H. Chalasani, Michael P. Hart
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. C. elegans aggregate in large clumps during feeding. Here, the authors find conserved autism-associated genes mediate distinct molecular and circuit signaling components that tune C. elegans feeding behavior from solitary to social feeding.