ArticleeLife2016
HSF-1 activates the ubiquitin proteasome system to promote non-apoptotic developmental cell death in C. elegans.
Article in eLife, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
What it found
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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
24 citing papers in PubMed, 36 citations in OpenAlex.
- Reduced Proteasome Degradation of HSF-1 Shifts Protein Stress Management With Age in Caenorhabditis elegans.Aging cell · 2026Article
- Article
- Non-apoptotic death of thebioRxiv : the preprint server for biology · 2025Article
- Activation of the aryl hydrocarbon receptor relieves acute pancreatitis via the RBX1/HSF1 pathway.Journal of inflammation (London, England) · 2025Article
- A default silencing mechanism restrains stress-induced genes inbioRxiv : the preprint server for biology · 2025Article
- CED-3 caspase promotes dismantling but not onset of non-apoptotic linker cell death inbioRxiv : the preprint server for biology · 2025Article
- An antisteatosis response regulated by oleic acid through lipid droplet-mediated ERAD enhancement.Science advances · 2023Article
- Modulation of the ubiquitin-proteasome system by marine natural products.Redox biology · 2021Review
- DNase II mediates a parthanatos-like developmental cell death pathway in Drosophila primordial germ cells.Nature communications · 2021Article
- The E3 ligase UBR2 regulates cell death under caspase deficiency via Erk/MAPK pathway.Cell death & disease · 2020Article
- Cell death in animal development.Development (Cambridge, England) · 2020Review
- After-Death Functions of Cell Death.The Yale journal of biology and medicine · 2019Review
- Cellular stress mechanisms of prenatal maternal stress: Heat shock factors and oxidative stress.Neuroscience letters · 2019Review
- Entosis Controls a Developmental Cell Clearance in C. elegans.Cell reports · 2019Article
- RAB-35 and ARF-6 GTPases Mediate Engulfment and Clearance Following Linker Cell-Type Death.Developmental cell · 2018Article
- Roles of heat shock factor 1 beyond the heat shock response.Cellular and molecular life sciences : CMLS · 2018Review
- EFF-1 fusogen promotes phagosome sealing during cell process clearance in Caenorhabditis elegans.Nature cell biology · 2018Article
- Sexual Dimorphism and Sex Differences inGenetics · 2018Article
- Article
- Rethinking HSF1 in Stress, Development, and Organismal Health.Trends in cell biology · 2017Review
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
Abstract
Apoptosis is a prominent metazoan cell death form. Yet, mutations in apoptosis regulators cause only minor defects in vertebrate development, suggesting that another developmental cell death mechanism exists. While some non-apoptotic programs have been molecularly characterized, none appear to control developmental cell culling. Linker-cell-type death (LCD) is a morphologically conserved non-apoptotic cell death process operating in Caenorhabditis elegans and vertebrate development, and is therefore a compelling candidate process complementing apoptosis. However, the details of LCD execution are not known. Here we delineate a molecular-genetic pathway governing LCD in C. elegans. Redundant activities of antagonistic Wnt signals, a temporal control pathway, and mitogen-activated protein kinase kinase signaling control heat shock factor 1 (HSF-1), a conserved stress-activated transcription factor. Rather than protecting cells, HSF-1 promotes their demise by activating components of the ubiquitin proteasome system, including the E2 ligase LET-70/UBE2D2 functioning with E3 components CUL-3, RBX-1, BTBD-2, and SIAH-1. Our studies uncover design similarities between LCD and developmental apoptosis, and provide testable predictions for analyzing LCD in vertebrates.
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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.