ArticlePLoS genetics2016
Loss of the Greatwall Kinase Weakens the Spindle Assembly Checkpoint.
Article in PLoS genetics, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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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
24 citing papers in PubMed, 45 citations in OpenAlex.
- The balance between B55α and Greatwall expression levels predicts sensitivity to Greatwall inhibition in cancer cells.Nature communications · 2025Article
- Protein-targeting reverse genetic approaches: the future of oocyte and preimplantation embryo research.Molecular human reproduction · 2025Review
- Deficiency ofFrontiers in cell and developmental biology · 2024Article
- Endosulfine alpha maintains spindle pole integrity by recruiting Aurora A during mitosis.BMC cancer · 2023Article
- Identification of PP2A-B55 targets uncovers regulation of emerin during nuclear envelope reassembly inOpen biology · 2023Article
- The MASTL/PP2A cell cycle kinase-phosphatase module restrains PI3K-Akt activity in an mTORC1-dependent manner.The EMBO journal · 2023Article
- Article
- Review
- Structural, enzymatic and spatiotemporal regulation of PP2A-B55 phosphatase in the control of mitosis.Frontiers in cell and developmental biology · 2022Review
- Spatiotemporal coordination of Greatwall-Endos-PP2A promotes mitotic progression.The Journal of cell biology · 2021Article
- Knockdown of Microtubule Associated Serine/threonine Kinase Like Expression Inhibits Gastric Cancer Cell Growth and Induces Apoptosis by Activation of ERK1/2 and Inactivation of NF-κB Signaling.Current medical science · 2021Article
- The Greatwall kinase safeguards the genome integrity by affecting the kinome activity in mitosis.Oncogene · 2020Article
- MASTL: A novel therapeutic target for Cancer Malignancy.Cancer medicine · 2020Review
- Recent advances in understanding the role of Cdk1 in the Spindle Assembly Checkpoint.F1000Research · 2020Review
- Multiple interaction nodes define the postreplication repair response to UV-induced DNA damage that is defective in melanomas and correlated with UV signature mutation load.Molecular oncology · 2020Article
- CDK2 regulates the NRF1/The Journal of cell biology · 2019Article
- CDK1-CCNB1 creates a spindle checkpoint-permissive state by enabling MPS1 kinetochore localization.The Journal of cell biology · 2019Article
- Phosphatases in Mitosis: Roles and Regulation.Biomolecules · 2019Review
- Protein phosphatases in the regulation of mitosis.The Journal of cell biology · 2019Review
- MASTL overexpression promotes chromosome instability and metastasis in breast cancer.Oncogene · 2018Article
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Greatwall kinase/Mastl is an essential gene that indirectly inhibits the phosphatase activity toward mitotic Cdk1 substrates. Here we show that although Mastl knockout (MastlNULL) MEFs enter mitosis, they progress through mitosis without completing cytokinesis despite the presence of misaligned chromosomes, which causes chromosome segregation defects. Furthermore, we uncover the requirement of Mastl for robust spindle assembly checkpoint (SAC) maintenance since the duration of mitotic arrest caused by microtubule poisons in MastlNULL MEFs is shortened, which correlates with premature disappearance of the essential SAC protein Mad1 at the kinetochores. Notably, MastlNULL MEFs display reduced phosphorylation of a number of proteins in mitosis, which include the essential SAC kinase MPS1. We further demonstrate that Mastl is required for multi-site phosphorylation of MPS1 as well as robust MPS1 kinase activity in mitosis. In contrast, treatment of MastlNULL cells with the phosphatase inhibitor okadaic acid (OKA) rescues the defects in MPS1 kinase activity, mislocalization of phospho-MPS1 as well as Mad1 at the kinetochore, and premature SAC silencing. Moreover, using in vitro dephosphorylation assays, we demonstrate that Mastl promotes persistent MPS1 phosphorylation by inhibiting PP2A/B55-mediated MPS1 dephosphorylation rather than affecting Cdk1 kinase activity. Our findings establish a key regulatory function of the Greatwall kinase/Mastl->PP2A/B55 pathway in preventing premature SAC silencing.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.