ArticlePLoS biology2022
A caspase-RhoGEF axis contributes to the cell size threshold for apoptotic death in developing Caenorhabditis elegans.
Article in PLoS biology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 10 citations in OpenAlex.
- Cell size modulates ferroptosis susceptibility.eLife · 2026Article
- Cell size modulates ferroptosis susceptibility.bioRxiv : the preprint server for biology · 2026Article
- Unequal segregation of mitochondria during asymmetric cell division contributes to cell fate divergence in sister cells in vivo.Nature communications · 2025Article
- Cell lineage-resolved embryonic morphological map reveals signaling associated with cell fate and size asymmetry.Nature communications · 2025Article
- Immunological Safety Evaluation of Exosomes Derived From Human Umbilical Cord Mesenchymal Stem Cells in Mice.Stem cells international · 2025Article
- Impact of embryo size on apoptosis inmicroPublication biology · 2025Article
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
A cell's size affects the likelihood that it will die. But how is cell size controlled in this context and how does cell size impact commitment to the cell death fate? We present evidence that the caspase CED-3 interacts with the RhoGEF ECT-2 in Caenorhabditis elegans neuroblasts that generate "unwanted" cells. We propose that this interaction promotes polar actomyosin contractility, which leads to unequal neuroblast division and the generation of a daughter cell that is below the critical "lethal" size threshold. Furthermore, we find that hyperactivation of ECT-2 RhoGEF reduces the sizes of unwanted cells. Importantly, this suppresses the "cell death abnormal" phenotype caused by the partial loss of ced-3 caspase and therefore increases the likelihood that unwanted cells die. A putative null mutation of ced-3 caspase, however, is not suppressed, which indicates that cell size affects CED-3 caspase activation and/or activity. Therefore, we have uncovered novel sequential and reciprocal interactions between the apoptosis pathway and cell size that impact a cell's commitment to the cell death fate.
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Registered trials
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