ArticleMolecular biology of the cell2015
Control of the spindle checkpoint by lateral kinetochore attachment and limited Mad1 recruitment.
Article in Molecular biology of the cell, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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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
5 citing papers in PubMed, 8 citations in OpenAlex.
- Signaling protein abundance modulates the strength of the spindle assembly checkpoint.Current biology : CB · 2023Article
- How Kinetochore Architecture Shapes the Mechanisms of Its Function.Current biology : CB · 2017Review
- Quantitative characterization of the auxin-inducible degron: a guide for dynamic protein depletion in single yeast cells.Scientific reports · 2017Article
- Spindle assembly checkpoint satisfaction occurs via end-on but not lateral attachments under tension.The Journal of cell biology · 2017Article
- Dual mechanisms regulate the recruitment of spindle assembly checkpoint proteins to the budding yeast kinetochore.Molecular biology of the cell · 2016Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
We observed the dynamic recruitment of spindle checkpoint proteins Mad1 and Bub1 to detached kinetochores in budding yeast using real-time live-cell imaging and quantified recruitment in fixed cells. After induced de novo kinetochore assembly at one pair of sister centromeres, Mad1 appeared after the kinetochore protein Mtw1. Detached kinetochores were not associated with the nuclear envelope, so Mad1 does not anchor them to nuclear pore complexes (NPCs). Disrupting Mad1's NPC localization increased Mad1 recruitment to detached sister kinetochores. Conversely, increasing the number of detached kinetochores reduced the amount of Mad1 per detached kinetochore. Bub1 also relocalized completely from the spindle to detached sister centromeres after kinetochore assembly. After their capture by microtubules, Mad1 and Bub1 progressively disappeared from kinetochores. Sister chromatids that arrested with a lateral attachment to one microtubule exhibited half the Mad1 of fully detached sisters. We propose that detached kinetochores compete with alternate binding sites in the nucleus to recruit Mad1 and Bub1 from available pools that are small enough to be fully depleted by just one pair of detached kinetochores and that lateral attachment licenses Mad1 removal from kinetochores after a kinetic delay.
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Registered trials
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