ArticlePLoS genetics2015
The Nuclear Matrix Protein Megator Regulates Stem Cell Asymmetric Division through the Mitotic Checkpoint Complex in Drosophila Testes.
Article in PLoS genetics, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Predominant Asymmetrical Stem Cell Fate Outcome Limits the Rate of Niche Succession in Human Colonic Crypts.EBioMedicine · 2018Trial
- Unusual modes of cell and nuclear divisions characterise Drosophila development.Biochemical Society transactions · 2024Review
- Cellular and molecular mechanisms of asymmetric stem cell division in tissue homeostasis.Genes to cells : devoted to molecular & cellular mechanisms · 2024Review
- An actomyosin network organizes niche morphology and responds to feedback from recruited stem cells.Current biology : CB · 2024Article
- An actomyosin network organizes niche morphology and responds to feedback from recruited stem cells.bioRxiv : the preprint server for biology · 2024Article
- Targeting MAD2 modulates stemness and tumorigenesis in human Gastric Cancer cell lines.Theranostics · 2020Article
- Review
- Whole-animal genome-wide RNAi screen identifies networks regulating male germline stem cells in Drosophila.Nature communications · 2016Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
In adult Drosophila testis, asymmetric division of germline stem cells (GSCs) is specified by an oriented spindle and cortically localized adenomatous coli tumor suppressor homolog 2 (Apc2). However, the molecular mechanism underlying these events remains unclear. Here we identified Megator (Mtor), a nuclear matrix protein, which regulates GSC maintenance and asymmetric division through the spindle assembly checkpoint (SAC) complex. Loss of Mtor function results in Apc2 mis-localization, incorrect centrosome orientation, defective mitotic spindle formation, and abnormal chromosome segregation that lead to the eventual GSC loss. Expression of mitotic arrest-deficient-2 (Mad2) and monopolar spindle 1 (Mps1) of the SAC complex effectively rescued the GSC loss phenotype associated with loss of Mtor function. Collectively our results define a new role of the nuclear matrix-SAC axis in regulating stem cell maintenance and asymmetric division.
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Registered trials
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