ArticlePLoS genetics2014
LIN-3/EGF promotes the programmed cell death of specific cells in Caenorhabditis elegans by transcriptional activation of the pro-apoptotic gene egl-1.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 26 citations in OpenAlex.
- Emerging roles of tsRNAs in programmed cell death and disease therapeutics: challenges, opportunities, and future directions.Non-coding RNA research · 2025Review
- Vacuolar HeLife · 2024Article
- SCAV-3 affects apoptotic cell degradation in Caenorhabditis elegans.FEBS open bio · 2023Article
- Repurposing the Killing Machine: Non-canonical Roles of the Cell Death Apparatus inFrontiers in cell and developmental biology · 2022Review
- ALG-2/AGO-DependentGenetics · 2019Article
- Ras/MAPK Modifier Loci Revealed by eQTL inG3 (Bethesda, Md.) · 2017Article
- miRNAs cooperate in apoptosis regulation duringGenes & development · 2017Article
- Modulation of Alpha-synuclein Expression and Associated Effects by MicroRNA Let-7 in TransgenicFrontiers in molecular neuroscience · 2017Article
- Epidermal Growth Factor Receptor Cell Survival Signaling Requires Phosphatidylcholine Biosynthesis.G3 (Bethesda, Md.) · 2016Article
- Article
- Programmed cell death and clearance of cell corpses in Caenorhabditis elegans.Cellular and molecular life sciences : CMLS · 2016Review
- Article
- Cell Death in C. elegans Development.Current topics in developmental biology · 2015Review
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2 authors at 2 institutions in 1 country.
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Abstract
Programmed cell death (PCD) is the physiological death of a cell mediated by an intracellular suicide program. Although key components of the PCD execution pathway have been identified, how PCD is regulated during development is poorly understood. Here, we report that the epidermal growth factor (EGF)-like ligand LIN-3 acts as an extrinsic signal to promote the death of specific cells in Caenorhabditis elegans. The loss of LIN-3 or its receptor, LET-23, reduced the death of these cells, while excess LIN-3 or LET-23 signaling resulted in an increase in cell deaths. Our molecular and genetic data support the model that the LIN-3 signal is transduced through LET-23 to activate the LET-60/RAS-MPK-1/ERK MAPK pathway and the downstream ETS domain-containing transcription factor LIN-1. LIN-1 binds to, and activates transcription of, the key pro-apoptotic gene egl-1, which leads to the death of specific cells. Our results provide the first evidence that EGF induces PCD at the whole organism level and reveal the molecular basis for the death-promoting function of LIN-3/EGF. In addition, the level of LIN-3/EGF signaling is important for the precise fine-tuning of the life-versus-death fate. Our data and the previous cell culture studies that say EGF triggers apoptosis in some cell lines suggest that the EGF-mediated modulation of PCD is likely conserved in C. elegans and humans.
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