ArticleCell death and differentiation2010
Transcriptional upregulation of both egl-1 BH3-only and ced-3 caspase is required for the death of the male-specific CEM neurons.
Article in Cell death and differentiation, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 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
17 citing papers in PubMed, 27 citations in OpenAlex.
- Pervasive homeobox gene function in the male-specific nervous system of Caenorhabditis elegans.Development (Cambridge, England) · 2025Article
- Structural and physiological functions ofHeliyon · 2024Review
- Neurogenesis in Caenorhabditis elegans.Genetics · 2024Review
- A genetic screen identifiesmicroPublication biology · 2024Article
- Role of transcription factors in apoptotic cells clearance.Frontiers in cell and developmental biology · 2023Review
- Repurposing the Killing Machine: Non-canonical Roles of the Cell Death Apparatus inFrontiers in cell and developmental biology · 2022Review
- T-Cell Factors as Transcriptional Inhibitors: Activities and Regulations in Vertebrate Head Development.Frontiers in cell and developmental biology · 2021Review
- Activity-Dependent Regulation of the Proapoptotic BH3-Only GeneG3 (Bethesda, Md.) · 2019Article
- EFF-1 fusogen promotes phagosome sealing during cell process clearance in Caenorhabditis elegans.Nature cell biology · 2018Article
- Sexual Dimorphism and Sex Differences inGenetics · 2018Article
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- Caenorhabditis elegans glp-4 Encodes a Valyl Aminoacyl tRNA Synthetase.G3 (Bethesda, Md.) · 2015Article
- Cell Death in C. elegans Development.Current topics in developmental biology · 2015Review
- Noncanonical cell death in the nematode Caenorhabditis elegans.Methods in enzymology · 2014Review
- Cell lineage and cell death: Caenorhabditis elegans and cancer research.Nature reviews. Cancer · 2011Review
- Six and Eya promote apoptosis through direct transcriptional activation of the proapoptotic BH3-only gene egl-1 in Caenorhabditis elegans.Proceedings of the National Academy of Sciences of the United States of America · 2010Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Most of the 131 cells that die during the development of a Caenorhabditis elegans hermaphrodite do so approximately 30 min after being generated. Furthermore, in these cells, the pro-caspase proCED-3 is inherited from progenitors and the transcriptional upregulation of the BH3-only gene egl-1 is thought to be sufficient for apoptosis induction. In contrast, the four CEM neurons, which die in hermaphrodites, but not males, die approximately 150 min after being generated. We found that in the CEMs, the transcriptional activation of both the egl-1 and ced-3 gene is necessary for apoptosis induction. In addition, we show that the Bar homeodomain transcription factor CEH-30 represses egl-1 and ced-3 transcription in the CEMs, thereby permitting their survival. Furthermore, we identified three genes, unc-86, lrs-1, and unc-132, which encode a POU homeodomain transcription factor, a leucyl-tRNA synthetase, and a novel protein with limited sequence similarity to the mammalian proto-oncoprotein and kinase PIM-1, respectively, that promote the expression of the ceh-30 gene in the CEMs. On the basis of these results, we propose that egl-1 and ced-3 transcription are coregulated in the CEMs to compensate for limiting proCED-3 levels, which most probably are a result of proCED-3 turn over. Similar coregulatory mechanisms for BH3-only proteins and pro-caspases may function in higher organisms to allow efficient apoptosis induction. Finally, we present evidence that the timing of the death of the CEMs is controlled by TRA-1 Gli, the terminal global regulator of somatic sexual fate in C. elegans.
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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.