Current biology : CB · 2026
The teneurin TEN-1 and its ligand LRON-11 support microbiota-induced neuroprotection and mechanosensory function in C. elegans.
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Li Jingxian, Castillo Juan Pablo, Cheng Shouqiang, Weathers Indya, Nawrocka Wioletta I, Alvarado Jorge, Zhao Minglei, Calixto Andrea, Özkan Engin, Araç Demet
Аннотация
Neuroprotection preserves neuronal structure and function by limiting damage and cell death, and diet-associated microbiota produce metabolites capable of influencing neuronal survival.1,2,3 In C. elegans, GABA and lactate produced by E. coli HT115 protect touch receptor neurons (TRNs) from MEC-4(d)-induced degeneration,2 and comparative gene-expression analysis identified the teneurin ten-1 as required for this microbiota-induced neuroprotection.3 Teneurins are evolutionarily conserved cell-adhesion molecules that regulate nervous system development, axon guidance, synapse formation, and neuronal connectivity primarily through trans-cellular interactions,4,5,6,7,8,9,10,11,12,13,14,15,16,17,18,19,20,21,22 and C. elegans, which contains a single teneurin gene, requires TEN-1 for normal nervous system development and tissue organization.5,13,14,23 Although vertebrate teneurins bind latrophilin G protein-coupled receptors,17,21,22,24 the C. elegans latrophilin homolog LAT-1 acts in parallel to TEN-1,25 leaving the receptor-ligand interactions that underlie TEN-1 function incompletely understood. Here, we identify Leucine-Rich Repeat Only 11 (LRON-11), a previously uncharacterized cell-adhesion molecule, as the ligand for TEN-1. The high-resolution cryoelectron microscopy (cryo-EM) structure of the TEN-1-LRON-11 complex reveals that the leucine-rich repeat domain of LRON-11 directly engages the transthyretin (TTR) domain of TEN-1 through a previously unrecognized interaction interface. Tissue-specific genetic analyses demonstrate that TEN-1 and LRON-11 are required for microbiota-mediated neuroprotection, and structure-guided interface mutations disrupting TEN-1-LRON-11 binding impair normal touch responses in vivo. Together, our findings establish a conserved receptor-ligand signaling axis that supports microbiota-mediated neuroprotection and normal touch responses, revealing how a single receptor-ligand interaction can support distinct neuronal functions.