ArticleCurrent biology : CB2025
Modulation of C. elegans behavior, fitness, and lifespan by AWB/ASH-dependent death perception.
Article in Current biology : CB, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
3 citing papers in PubMed.
- Defense against parasites covaries with reproductive timing, not with resistance.PLoS pathogens · 2026Article
- Parasite defense covaries with reproductive timing, not with resistance.bioRxiv : the preprint server for biology · 2026Article
- Caenorhabditis elegans as an experimental model for resilience-boosting microbiota interventions in nonmodel ectotherms.FEMS microbiology reviews · 2026Review
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4 authors.
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Abstract
The ability of the nervous system to initiate intricate goal-directed behaviors in response to environmental stimuli is essential for metazoan survival. In this study, we demonstrate that the nematode Caenorhabditis elegans perceives and reacts to dead conspecifics. The exposure to C. elegans corpses, as well as corpse lysates, activates sensory neurons AWB and ASH, triggering a glutamate- and acetylcholine-dependent signaling cascade that regulates both immediate (aversion) and long-term (survival) responses to the presence of a death signature. We identify increased adenosine monophosphate (AMP) and histidine concentrations as potential chemical fingerprints for the presence of metazoan corpses and show that death cue sensing by AWB and ASH leads to physiological changes that promote reproduction at the expense of lifespan. Our findings illuminate a signaling paradigm that allows organisms to detect and interpret the environmental enrichment of intracellular metabolites as a death cue.
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