ArticleeLife2020
The copy-number and varied strengths of MELT motifs in Spc105 balance the strength and responsiveness of the spindle assembly checkpoint.
Article in eLife, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
10 citing papers in PubMed, 17 citations in OpenAlex.
- Interplay of kinetochores and catalysts drives rapid assembly of the mitotic checkpoint complex.Nature communications · 2025Article
- Signaling protein abundance modulates the strength of the spindle assembly checkpoint.Current biology : CB · 2023Article
- A bifunctional kinase-phosphatase module balances mitotic checkpoint strength and kinetochore-microtubule attachment stability.The EMBO journal · 2023Article
- Principles and dynamics of spindle assembly checkpoint signalling.Nature reviews. Molecular cell biology · 2023Review
- BubR1 recruitment to the kinetochore via Bub1 enhances spindle assembly checkpoint signaling.Molecular biology of the cell · 2022Article
- Aurora B phosphorylates Bub1 to promote spindle assembly checkpoint signaling.Current biology : CB · 2022Article
- Zombies Never Die: The Double Life Bub1 Lives in Mitosis.Frontiers in cell and developmental biology · 2022Review
- Kre28-Spc105 interaction is essential for Spc105 loading at the kinetochore.Open biology · 2022Article
- Spindle assembly checkpoint activation and silencing at kinetochores.Seminars in cell & developmental biology · 2021Review
- Mitotic checkpoint defects: en route to cancer and drug resistance.Chromosome research : an international journal on the molecular, supramolecular and evolutionary aspects of chromosome biology · 2021Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
Abstract
During mitosis, the Spindle Assembly Checkpoint (SAC) maintains genome stability while also ensuring timely anaphase onset. To maintain genome stability, the SAC must be strong to delay anaphase even if just one chromosome is unattached, but for timely anaphase onset, it must promptly respond to silencing mechanisms. How the SAC meets these potentially antagonistic requirements is unclear. Here we show that the balance between SAC strength and responsiveness is determined by the number of 'MELT' motifs in the kinetochore protein Spc105/KNL1 and their Bub3-Bub1 binding affinities. Many strong MELT motifs per Spc105/KNL1 minimize chromosome missegregation, but too many delay anaphase onset. We demonstrate this by constructing a Spc105 variant that trades SAC responsiveness for much more accurate chromosome segregation. We propose that the necessity of balancing SAC strength and responsiveness drives the dual evolutionary trend of the amplification of MELT motif number, but degeneration of their functionally optimal amino acid sequence.
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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.