ArticleThe Journal of cell biology2020
Mps1-mediated release of Mad1 from nuclear pores ensures the fidelity of chromosome segregation.
Article in The Journal of cell biology, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Sustainable integrative cell biology: CENP-C is guilty by association.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2025Article
- Article
- LncRNA938/ TAF9/TTK axis promotes EMT and serves as a therapeutic target in hepatoblastoma.Journal of translational medicine · 2025Article
- Conserved signalling functions for Mps1, Mad1 and Mad2 in the Cryptococcus neoformans spindle checkpoint.PLoS genetics · 2024Article
- Fission yeast essential nuclear pore protein Nup211 regulates the expression of genes involved in cytokinesis.PloS one · 2024Article
- Kinetochore-catalyzed MCC formation: A structural perspective.IUBMB life · 2023Article
- Spindle assembly checkpoint activation and silencing at kinetochores.Seminars in cell & developmental biology · 2021Review
- Rashomon at the kinetochore: Function(s) of the Mad1-cyclin B1 complex.The Journal of cell biology · 2020Article
- Spindle checkpoint: trapped by the corona, cyclin B1 goes MAD.The EMBO journal · 2020Article
- Cyclin B1-Cdk1 facilitates MAD1 release from the nuclear pore to ensure a robust spindle checkpoint.The Journal of cell biology · 2020Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The spindle assembly checkpoint (SAC) relies on the recruitment of Mad1-C-Mad2 to unattached kinetochores but also on its binding to Megator/Tpr at nuclear pore complexes (NPCs) during interphase. However, the molecular underpinnings controlling the spatiotemporal redistribution of Mad1-C-Mad2 as cells progress into mitosis remain elusive. Here, we show that activation of Mps1 during prophase triggers Mad1 release from NPCs and that this is required for kinetochore localization of Mad1-C-Mad2 and robust SAC signaling. We find that Mps1 phosphorylates Megator/Tpr to reduce its interaction with Mad1 in vitro and in Drosophila cells. Importantly, preventing Mad1 from binding to Megator/Tpr restores Mad1 accumulation at kinetochores, the fidelity of chromosome segregation, and genome stability in larval neuroblasts of mps1-null mutants. Our findings demonstrate that the subcellular localization of Mad1 is tightly coordinated with cell cycle progression by kinetochore-extrinsic activity of Mps1. This ensures that both NPCs in interphase and kinetochores in mitosis can generate anaphase inhibitors to efficiently preserve genomic stability.
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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.