ArticleGenetics2016
Programmed Cell Death During Caenorhabditis elegans Development.
Article in Genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 72 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
72 citing papers in PubMed.
- Tagging of C. elegans apoptosis activator EGL-1 BH3-only reveals CED-9 BCL-2-dependent mitochondrial localization and dynamic control of EGL-1 synthesis and degradation in vivo.Cell death and differentiation · 2026Article
- Endogenous expression and subcellular localization of core apoptosis regulators reveal key differences between embryonic and germline apoptosis in C. elegans.Cell death and differentiation · 2026Article
- Endogenous Expression and Subcellular Localization of Core Apoptosis Regulators Reveal Key Differences Between Embryonic and Germline Apoptosis in C. elegans.Research square · 2026Article
- Plant caspase-like proteins: from function identification to application in winter rapeseed genetic breeding.Frontiers in plant science · 2026Review
- Fluorescent protein tagging of C. elegans core apoptosis pathway components reveals mitochondrial localization of CED-9 Bcl-2, CED-4 Apaf1 and CED-3 Caspase in non-apoptotic and apoptotic cells.Cell death and differentiation · 2026Article
- From nematode to Nobel: How community-shared resources fueled the rise ofProceedings of the National Academy of Sciences of the United States of America · 2025Article
- EOR-1/PLZF promotes WAH-1/AIF-dependent compartment-specific corpse clearance.Cell death discovery · 2025Article
- Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo.Nature communications · 2025Article
- The replicative helicase CMG is required for the divergence of cell fates during asymmetric cell division in vivo.Nature communications · 2024Article
- Extracellular vesicles.Genetics · 2024Review
- Ferroptosis regulation by Cap'n'collar family transcription factors.The Journal of biological chemistry · 2024Review
- Actomyosin-mediated apical constriction promotes physiological germ cell death in C. elegans.PLoS biology · 2024Article
- Advancing insights into microgravity induced muscle changes using Caenorhabditis elegans as a model organism.NPJ microgravity · 2024Review
- Vacuolar HeLife · 2024Article
- Neurons dispose of hyperactive kinesin into glial cells for clearance.The EMBO journal · 2024Article
- Intercellular contact and cargo transfer between Müller glia and to microglia precede apoptotic cell clearance in the developing retina.Development (Cambridge, England) · 2024Article
- A genetic screen identifiesmicroPublication biology · 2024Article
- Article
- Getting there in one piece: The Rac pathway prevents cell fragmentation in a nonprotrusively migrating leader cell during organogenesis.bioRxiv : the preprint server for biology · 2023Article
- Intercellular contact and cargo transfer between Müller glia and to microglia precede apoptotic cell clearance in the developing retina.bioRxiv : the preprint server for biology · 2023Article
12 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors.
Funding
Abstract
Programmed cell death is an integral component of Caenorhabditis elegans development. Genetic and reverse genetic studies in C. elegans have led to the identification of many genes and conserved cell death pathways that are important for the specification of which cells should live or die, the activation of the suicide program, and the dismantling and removal of dying cells. Molecular, cell biological, and biochemical studies have revealed the underlying mechanisms that control these three phases of programmed cell death. In particular, the interplay of transcriptional regulatory cascades and networks involving multiple transcriptional regulators is crucial in activating the expression of the key death-inducing gene egl-1 and, in some cases, the ced-3 gene in cells destined to die. A protein interaction cascade involving EGL-1, CED-9, CED-4, and CED-3 results in the activation of the key cell death protease CED-3, which is tightly controlled by multiple positive and negative regulators. The activation of the CED-3 caspase then initiates the cell disassembly process by cleaving and activating or inactivating crucial CED-3 substrates; leading to activation of multiple cell death execution events, including nuclear DNA fragmentation, mitochondrial elimination, phosphatidylserine externalization, inactivation of survival signals, and clearance of apoptotic cells. Further studies of programmed cell death in C. elegans will continue to advance our understanding of how programmed cell death is regulated, activated, and executed in general.
Indexed as
Identifiers
What OpenQuestion holds
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.