ArticleStem cell reports2023
Stress-induced reversible cell-cycle arrest requires PRC2/PRC1-mediated control of mitophagy in Drosophila germline stem cells and human iPSCs.
Article in Stem cell reports, 2023. 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.
- Natural Genetic Variation Impacts Stress-Induced Quiescence and Regeneration in Response to Rapamycin.Cells · 2026Article
- H2AK119ub dynamics control hair follicle stem cell quiescence.Nature communications · 2025Article
- Rapamycin Differentially Impacts Germline Stem Cell Quiescence Across Diverse Genetic Backgrounds ofbioRxiv : the preprint server for biology · 2025Article
- Mitochondria - the CEO of the cell.Journal of cell science · 2025Review
- TNF-α-Induced KAT2A Impedes BMMSC Quiescence by Mediating Succinylation of the Mitophagy-Related Protein VCP.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024Article
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Authors and funding
17 authors at 2 institutions in 2 countries.
Funding
Abstract
Following acute genotoxic stress, both normal and tumorous stem cells can undergo cell-cycle arrest to avoid apoptosis and later re-enter the cell cycle to regenerate daughter cells. However, the mechanism of protective, reversible proliferative arrest, "quiescence," remains unresolved. Here, we show that mitophagy is a prerequisite for reversible quiescence in both irradiated Drosophila germline stem cells (GSCs) and human induced pluripotent stem cells (hiPSCs). In GSCs, mitofission (Drp1) or mitophagy (Pink1/Parkin) genes are essential to enter quiescence, whereas mitochondrial biogenesis (PGC1α) or fusion (Mfn2) genes are crucial for exiting quiescence. Furthermore, mitophagy-dependent quiescence lies downstream of mTOR- and PRC2-mediated repression and relies on the mitochondrial pool of cyclin E. Mitophagy-dependent reduction of cyclin E in GSCs and in hiPSCs during mTOR inhibition prevents the usual G1/S transition, pushing the cells toward reversible quiescence (G0). This alternative method of G1/S control may present new opportunities for therapeutic purposes.
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Registered trials
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