A nerve-signal receptor has opposite effects on worm survival
Experiments with two bacterial strains found that the receptor’s effects on early deaths depended on insulin receptor activity in the worms.
Our read
Mechanisms- Studied:
- Experiments in Caenorhabditis elegans worms, against worms with normal insulin receptor function
- What changed:
- NMUR-1 reduced early deaths with normal insulin receptor function but increased them with reduced function on OP50 bacteria
- The catch:
- Genetic and gene-activity results provide indirect evidence for the proposed receptor-signaling buffering mechanism
- Why it’s aging research:
- It measures how long life or healthy life lasts.
Editor of record: Boris Djordjevic · AgingResearch.News
In experiments with Caenorhabditis elegans worms, researchers compared survival on two strains of Escherichia coli bacteria at 25 degrees Celsius. Worms fed strain OP50 suffered more early deaths with swollen pharynges, muscular feeding organs, than worms fed CS180. Bacteria accumulated in this tissue.
NMUR-1, a protein that receives nerve-cell signals, reduced these deaths on OP50 when insulin receptor function was normal. But it increased them when mutations reduced the activity of DAF-2, the worms’ insulin receptor. Neither effect occurred on CS180. NMUR-1 acted in sensory nerve cells, and its opposing effects depended on DAF-16, a protein that controls gene activity. The authors proposed that NMUR-1 buffers insulin receptor signaling, helping maintain feeding-organ health and survival in response to particular bacteria.
Why it matters
Microbial environments influence worm lifespan. The study addresses how nerve-cell signals may help worms adjust a lifespan-related signaling system to the bacteria around them.
Caveats
These laboratory experiments tested worms under defined bacterial conditions, not people. The buffering mechanism is the authors’ interpretation of genetic and gene-activity results.
The paper
Wayne State University
PLOS Genetics, Jun 11, 2026, Open access
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