ArticleNature communications2025
Interplay of kinetochores and catalysts drives rapid assembly of the mitotic checkpoint complex.
Article in Nature communications, 2025. 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.
- Mitotic error correction and the spindle assembly checkpoint: a tension-filled relationship.Cell cycle (Georgetown, Tex.) · 2026Review
- Structure and function of the outer kinetochore.Nature reviews. Molecular cell biology · 2026Review
- BubR1 TPR domain supports the mitotic checkpoint by promoting MCC formation and MCC-APC/C interaction.Communications biology · 2026Article
- Network architecture determines delay robustness in the spindle assembly checkpoint.Scientific reports · 2026Article
- Tumor cell cycle regulation: integrated perspective of stage characteristics, regulatory networks, and signaling pathway intervention strategies.Molecular biomedicine · 2026Review
- Delayed Signaling in Mitotic Checkpoints: Biological Mechanisms and Modeling Perspectives.Biology · 2026Review
- Oocyte Kinetochores at the Nexus of Meiotic Drive and Segregation Fidelity.Advances in experimental medicine and biology · 2026Review
- Molecular mechanism of Mad2 conformational conversion promoted by the Mad2-interaction motif of Cdc20.Protein science : a publication of the Protein Society · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The spindle assembly checkpoint (SAC) ensures mitotic exit occurs only after sister chromatid biorientation, but how this coordination is mechanistically achieved remains unclear. Kinetochores, the megadalton complexes linking chromosomes to spindle microtubules, contribute to SAC signaling. However, whether they act solely as docking platforms or actively promote the co-orientation of SAC catalysts such as MAD1:MAD2 and BUB1:BUB3 remains unresolved. Here, we reconstitute kinetochores and SAC signaling in vitro to address this question. We engineer recombinant kinetochore particles that recruit core SAC components and trigger checkpoint signaling upon Rapamycin induction, and test their function using a panel of targeted mutants. At approximately physiological concentrations of SAC proteins, kinetochores are essential for efficient mitotic checkpoint complex (MCC) assembly, the key effector of SAC signaling. Our results suggest that kinetochores serve not only as structural hubs but also as catalytic platforms that concentrate and spatially organize SAC components to accelerate MCC formation and ensure timely checkpoint activation.
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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.