Neuropeptide receptor NMUR-1 buffers insulin signalling to modulate C. elegans survival on different bacteria
A PLOS Genetics study shows that the neuromedin U receptor NMUR-1 tempers insulin pathway activity in C. elegans, shaping how the worm survives on distinct bacterial food sources.
Researchers publishing in PLOS Genetics report that the neuropeptide receptor NMUR-1 — the C. elegans homologue of vertebrate neuromedin U receptors — acts as a buffer of insulin receptor signalling to modulate worm survival when grown on different strains of Escherichia coli.
The study, by Sifoglu, Pereira, DeGregory, Shah, and colleagues, shows that wild-type C. elegans raised on the commonly used E. coli strain OP50 experience more early deaths than animals raised on an alternative strain, CS180. Early deaths on OP50 were associated with swollen pharynges caused by bacterial accumulation. The authors demonstrate that NMUR-1 signalling adjusts the activity of the canonical insulin/IGF-1 signalling (IIS) pathway in a bacteria-dependent manner, with loss of nmur-1 altering the balance between survival and early mortality in a food-context-specific way.
The findings extend understanding of how neuroendocrine circuits integrate microbial environmental signals to tune lifespan and health-span related traits in C. elegans. The IIS pathway is highly conserved across metazoans, and C. elegans is an established model for studying the genetics of ageing, development, and host-microbe interaction. The paper was published in PLOS Genetics on 11 June 2026. As model-organism research, the results do not translate directly to human biology without further investigation.
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Primary source PLOS Genetics · 2026-06-11The neuropeptide neuromedin U receptor NMUR-1 buffers insulin receptor signaling in bacteria-dependent C. elegans survival