ArticleMolecular biology of the cell2023
The role of kinetochore dynein in checkpoint silencing is restricted to disassembly of the corona.
Article in Molecular biology of the cell, 2023. 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, 12 citations in OpenAlex.
- Structure and function of the outer kinetochore.Nature reviews. Molecular cell biology · 2026Review
- Tiny Yeast Comet 1-Dependent Polymers Suppress Taxol-Stabilized Microtubule Depolymerization Induced by Ice-Cold CaClInternational journal of molecular sciences · 2026Article
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- Kinetochore dynein is sufficient to biorient chromosomes and remodel the outer kinetochore.Nature communications · 2024Article
- A conserved CENP-E region mediates BubR1-independent recruitment to the outer corona at mitotic onset.Current biology : CB · 2024Article
- Role of spindle assembly checkpoint proteins in gametogenesis and embryogenesis.Frontiers in cell and developmental biology · 2024Review
- CENP-E activation by Aurora A and B controls kinetochore fibrous corona disassembly.Nature communications · 2023Article
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
During mitosis, kinetochore-microtubule attachments are monitored by a molecular surveillance system known as the spindle assembly checkpoint. The prevailing model posits that dynein evicts checkpoint proteins (e.g., Mad1, Mad2) from stably attached kinetochores by transporting them away from kinetochores, thus contributing to checkpoint silencing. However, the mechanism by which dynein performs this function, and its precise role in checkpoint silencing remain unresolved. Here, we find that dynein's role in checkpoint silencing is restricted to evicting checkpoint effectors from the fibrous corona, and not the outer kinetochore. Dynein evicts these molecules from the corona in a manner that does not require stable, end-on microtubule attachments. Thus, by disassembling the corona through indiscriminate microtubule encounters, dynein primes the checkpoint signaling apparatus so it can respond to stable end-on microtubule attachments and permit cells to progress through mitosis. Accordingly, we find that dynein function in checkpoint silencing becomes largely dispensable in cells in which checkpoint effectors are excluded from the corona.
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