ArticleDevelopmental cell2020
Non-Canonical Caspase Activity Antagonizes p38 MAPK Stress-Priming Function to Support Development.
Article in Developmental cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 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
23 citing papers in PubMed, 41 citations in OpenAlex.
- Reductive death is averted by a conserved de novo lipogenic switch.Molecular cell · 2026Article
- Worming out defence strategies: mechanisms of immunity through the lens of genetic screens in C. elegans.Heredity · 2026Review
- AScience signaling · 2026Article
- Intersections between proteostasis and immunity: insights from Caenorhabditis elegans.Disease models & mechanisms · 2026Review
- Loofah suppresses cell death in long-lived Drosophila hindgut enterocytes.Development (Cambridge, England) · 2025Article
- CED-3 caspase promotes dismantling but not onset of non-apoptotic linker cell death inbioRxiv : the preprint server for biology · 2025Article
- Differential impacts of ribosomal protein haploinsufficiency on mitochondrial function.The Journal of cell biology · 2025Article
- Xeroderma pigmentosum protein XPD controls caspase-mediated stress responses.Nature communications · 2024Article
- Lysosome-related organelle integrity suppresses TIR-1 aggregation to restrain toxic propagation of p38 innate immunity.Cell reports · 2024Article
- UPReLife · 2024Article
- Cutting through stress.Nature metabolism · 2024Article
- Proteolytic activation of fatty acid synthase signals pan-stress resolution.Nature metabolism · 2024Article
- Caspase 3 exhibits a yeast metacaspase proteostasis function that protects mitochondria from toxic TDP43 aggregates.Microbial cell (Graz, Austria) · 2023Article
- Modulating p38 MAPK signaling by proteostasis mechanisms supports tissue integrity during growth and aging.Nature communications · 2023Article
- Caspases help to spread the message via extracellular vesicles.The FEBS journal · 2023Review
- UBR5 is a novel regulator of WNK1 stability.American journal of physiology. Cell physiology · 2022Article
- Non-apoptotic activation of Drosophila caspase-2/9 modulates JNK signaling, the tumor microenvironment, and growth of wound-like tumors.Cell reports · 2022Article
- C. elegans: out on an evolutionary limb.Immunogenetics · 2022Review
- Antagonistic fungal enterotoxins intersect at multiple levels with host innate immune defences.PLoS genetics · 2021Article
- Diversity and versatility of p38 kinase signalling in health and disease.Nature reviews. Molecular cell biology · 2021Review
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
Abstract
Recent studies have revealed non-canonical activities of apoptotic caspases involving specific modulation of gene expression, such as limiting asymmetric divisions of stem-like cell types. Here we report that CED-3 caspase negatively regulates an epidermal p38 stress-responsive MAPK pathway to promote larval development in C. elegans. We show that PMK-1 (p38 MAPK) primes animals for encounters with hostile environments at the expense of retarding post-embryonic development. CED-3 counters this function by directly cleaving PMK-1 to promote development. Moreover, we found that CED-3 and PMK-1 oppose each other to balance developmental and stress-responsive gene expression programs. Specifically, expression of more than 300 genes is inversely regulated by CED-3 and PMK-1. Analyses of these genes showed enrichment for epidermal stress-responsive factors, including the fatty acid synthase FASN-1, anti-microbial peptides, and genes involved in lethargus states. Our findings demonstrate a non-canonical role for a caspase in promoting development by limiting epidermal stress response programs.
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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.