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

Nat Commun. 2024 Oct 28;15(1):9301. doi: 10.1038/s41467-024-53590-x.

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.

MeSH terms

  • Animals
  • Autistic Disorder* / genetics
  • Caenorhabditis elegans Proteins* / genetics
  • Caenorhabditis elegans Proteins* / metabolism
  • Caenorhabditis elegans* / genetics
  • Caenorhabditis elegans* / physiology
  • Cell Adhesion Molecules, Neuronal
  • Chemoreceptor Cells / metabolism
  • Feeding Behavior* / physiology
  • Glutamic Acid / metabolism
  • Neural Cell Adhesion Molecules / genetics
  • Neural Cell Adhesion Molecules / metabolism
  • Receptors, AMPA / genetics
  • Receptors, AMPA / metabolism
  • Social Behavior*

Substances

  • Caenorhabditis elegans Proteins
  • nrx-1 protein, C elegans
  • Glutamic Acid
  • glr-1 protein, C elegans
  • Receptors, AMPA
  • Neural Cell Adhesion Molecules
  • Cell Adhesion Molecules, Neuronal