ArticleStem cell reports2015
The Spindle Assembly Checkpoint Safeguards Genomic Integrity of Skeletal Muscle Satellite Cells.
Article in Stem cell reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
7 citing papers in PubMed, 13 citations in OpenAlex.
- On the role of p53 in the cellular response to aneuploidy.Cell reports · 2021Article
- Premature aging syndrome showing random chromosome number instabilities with CDC20 mutation.Aging cell · 2020Article
- Agent-based model illustrates the role of the microenvironment in regeneration in healthy and mdx skeletal muscle.Journal of applied physiology (Bethesda, Md. : 1985) · 2018Article
- Chromosome integrity checkpoints in stem and progenitor cells: transitions upon differentiation, pathogenesis, and aging.Cellular and molecular life sciences : CMLS · 2018Review
- The Spindle Assembly Checkpoint Is Required for Hematopoietic Progenitor Cell Engraftment.Stem cell reports · 2017Article
- Satellite Cells in Muscular Dystrophy - Lost in Polarity.Trends in molecular medicine · 2016Review
- Dystrophin expression in muscle stem cells regulates their polarity and asymmetric division.Nature medicine · 2015Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
To ensure accurate genomic segregation, cells evolved the spindle assembly checkpoint (SAC), whose role in adult stem cells remains unknown. Inducible perturbation of a SAC kinase, Mps1, and its downstream effector, Mad2, in skeletal muscle stem cells shows the SAC to be critical for normal muscle growth, repair, and self-renewal of the stem cell pool. SAC-deficient muscle stem cells arrest in G1 phase of the cell cycle with elevated aneuploidy, resisting differentiation even under inductive conditions. p21(CIP1) is responsible for these SAC-deficient phenotypes. Despite aneuploidy's correlation with aging, we find that aged proliferating muscle stem cells display robust SAC activity without elevated aneuploidy. Thus, muscle stem cells have a two-step mechanism to safeguard their genomic integrity. The SAC prevents chromosome missegregation and, if it fails, p21(CIP1)-dependent G1 arrest limits cellular propagation and tissue integration. These mechanisms ensure that muscle stem cells with compromised genomes do not contribute to tissue homeostasis.
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Registered trials
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