ArticleScientific reports2022
Cold shock induces a terminal investment reproductive response in C. elegans.
Article in Scientific reports, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- An mTORC2-Lipid Signaling Axis Controls Stress-Induced Organismal Death.Research square · 2026Article
- Cold and lithium delay forgetting of olfactory memories in Caenorhabditis elegans.Nature neuroscience · 2026Article
- Host Transcriptomics Reveal Reduction in Defence-Reproduction Trade-Offs During Coinfection.Molecular ecology · 2025Article
- SQST-1/p62-regulated SKN-1/Nrf mediates a phagocytic stress response via transcriptional activation of lyst-1/LYST.PLoS genetics · 2025Article
- Temperature Effects on Expression Levels ofInternational journal of molecular sciences · 2024Article
- GPCR signaling regulates severe stress-induced organismic death in Caenorhabditis elegans.Aging cell · 2023Article
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2 authors at 1 institution in 1 country.
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Abstract
Challenges from environmental stressors have a profound impact on many life-history traits of an organism, including reproductive strategy. Examples across multiple taxa have demonstrated that maternal reproductive investment resulting from stress can improve offspring survival; a form of matricidal provisioning when death appears imminent is known as terminal investment. Here we report a reproductive response in the nematode Caenorhabditis elegans upon exposure to acute cold shock at 2 °C, whereby vitellogenic lipid movement from the soma to the germline appears to be massively upregulated at the expense of parental survival. This response is dependent on functional TAX-2; TAX-4 cGMP-gated channels that are part of canonical thermosensory mechanisms in worms and can be prevented in the presence of activated SKN-1/Nrf2, the master stress regulator. Increased maternal provisioning promotes improved embryonic cold shock survival, which is notably suppressed in animals with impaired vitellogenesis. These findings suggest that cold shock in C. elegans triggers terminal investment to promote progeny fitness at the expense of parental survival and may serve as a tractable model for future studies of stress-induced progeny plasticity.
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