ArticleBMC cell biology2016
Long-term recovery from acute cold shock in Caenorhabditis elegans.
Article in BMC cell biology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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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Who cites it
21 citing papers in PubMed, 43 citations in OpenAlex.
- An mTORC2-Lipid Signaling Axis Controls Stress-Induced Organismal Death.Research square · 2026Article
- Reprograming gene expression in 'hibernating'eLife · 2025Article
- High-throughput developmental assay of cold tolerance inmicroPublication biology · 2025Article
- Cell non-autonomous signaling through the conserved C. elegans glycoprotein hormone receptor FSHR-1 regulates cholinergic neurotransmission.PLoS genetics · 2024Article
- Floxuridine supports UPS independent of germline signaling and proteostasis regulators via involvement of detoxification in C. elegans.PLoS genetics · 2024Article
- Effect of chronic cold stress on gut microbial diversity, intestinal inflammation and pyroptosis in mice.Journal of physiology and biochemistry · 2024Article
- Worm-Based Diagnosis Combining Microfluidics toward Early Cancer Screening.Micromachines · 2024Review
- The effect of common paralytic agents used for fluorescence imaging on redox tone and ATP levels in Caenorhabditis elegans.PloS one · 2024Article
- Cold Tolerance in the Nematode Caenorhabditis elegans.Advances in experimental medicine and biology · 2024Review
- Oxygen is toxic in the cold inFrontiers in physiology · 2024Article
- Cold temperature extends longevity and prevents disease-related protein aggregation through PA28γ-induced proteasomes.Nature aging · 2023Article
- High-throughput submicron-resolution microscopy ofiScience · 2023Article
- An unbiased, automated platform for scoring dopaminergic neurodegeneration inbioRxiv : the preprint server for biology · 2023Article
- An unbiased, automated platform for scoring dopaminergic neurodegeneration in C. elegans.PloS one · 2023Article
- Ferritin-mediated iron detoxification promotes hypothermia survival in Caenorhabditis elegans and murine neurons.Nature communications · 2022Article
- Cold shock induces a terminal investment reproductive response in C. elegans.Scientific reports · 2022Article
- Cold Survival and Its Molecular Mechanisms in a Locally Adapted Nematode Population.Genome biology and evolution · 2021Article
- Deep learning-enabled analysis reveals distinct neuronal phenotypes induced by aging and cold-shock.BMC biology · 2020Article
- Stress and timing associated withHeliyon · 2020Article
- Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
backgroundAnimals are exposed to a wide range of environmental stresses that can cause potentially fatal cellular damage. The ability to survive the period of stress as well as to repair any damage incurred is essential for fitness. Exposure to 2 °C for 24 h or longer is rapidly fatal to the nematode Caenorhabditis elegans, but the process of recovery from a shorter, initially non-lethal, cold shock is poorly understood.
resultsWe report that cold shock of less than 12-hour duration does not initially kill C. elegans, but these worms experience a progression of devastating phenotypes over the next 96 h that correlate with their eventual fate: successful recovery from the cold shock and survival, or failure to recover and death. Cold-shocked worms experience a marked loss of pigmentation, decrease in the size of their intestine and gonads, and disruption to the vulva. Those worms who will successfully recover from the cold shock regain their pigmentation and much of the integrity of their intestine and gonads. Those who will die do so with a distinct phenotype from worms dying during or immediately following cold shock, suggesting independent mechanisms. Worms lacking the G-protein coupled receptor FSHR-1 are resistant to acute death from longer cold shocks, and are more successful in their recovery from shorter sub-lethal cold shocks.
conclusionsWe have defined two distinct phases of death associated with cold shock and described a progression of phenotypes that accompanies the course of recovery from that cold shock. The G-protein coupled receptor FSHR-1 antagonizes these novel processes of damage and recovery.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.