ArticlePLoS genetics2020
PIG-1 MELK-dependent phosphorylation of nonmuscle myosin II promotes apoptosis through CES-1 Snail partitioning.
Article in PLoS genetics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 21 citations in OpenAlex.
- 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
- Impact of embryo size on apoptosis inmicroPublication biology · 2025Article
- The replicative helicase CMG is required for the divergence of cell fates during asymmetric cell division in vivo.Nature communications · 2024Article
- Actomyosin-mediated apical constriction promotes physiological germ cell death in C. elegans.PLoS biology · 2024Article
- Vacuolar HeLife · 2024Article
- Control of successive unequal cell divisions by neural cell fate regulators determines embryonic neuroblast cell size.Development (Cambridge, England) · 2024Article
- Article
- Caenorhabditis elegans for research on cancer hallmarks.Disease models & mechanisms · 2023Article
- A caspase-RhoGEF axis contributes to the cell size threshold for apoptotic death in developing Caenorhabditis elegans.PLoS biology · 2022Article
- Repurposing the Killing Machine: Non-canonical Roles of the Cell Death Apparatus inFrontiers in cell and developmental biology · 2022Review
- Wnt Signaling Induces Asymmetric Dynamics in the Actomyosin Cortex of theFrontiers in cell and developmental biology · 2021Article
- Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The mechanism(s) through which mammalian kinase MELK promotes tumorigenesis is not understood. We find that the C. elegans orthologue of MELK, PIG-1, promotes apoptosis by partitioning an anti-apoptotic factor. The C. elegans NSM neuroblast divides to produce a larger cell that differentiates into a neuron and a smaller cell that dies. We find that in this context, PIG-1 MELK is required for partitioning of CES-1 Snail, a transcriptional repressor of the pro-apoptotic gene egl-1 BH3-only. pig-1 MELK is controlled by both a ces-1 Snail- and par-4 LKB1-dependent pathway, and may act through phosphorylation and cortical enrichment of nonmuscle myosin II prior to neuroblast division. We propose that pig-1 MELK-induced local contractility of the actomyosin network plays a conserved role in the acquisition of the apoptotic fate. Our work also uncovers an auto-regulatory loop through which ces-1 Snail controls its own activity through the formation of a gradient of CES-1 Snail protein.
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