ArticleMolecular biology of the cell2008
Different levels of Bfa1/Bub2 GAP activity are required to prevent mitotic exit of budding yeast depending on the type of perturbations.
Article in Molecular biology of the cell, 2008. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 15 citations in OpenAlex.
- Article
- Article
- Review
- Budding YeastG3 (Bethesda, Md.) · 2018Article
- Colletotrichum orbiculare Regulates Cell Cycle G1/S Progression via a Two-Component GAP and a GTPase to Establish Plant Infection.The Plant cell · 2015Article
- From START to FINISH: computational analysis of cell cycle control in budding yeast.NPJ systems biology and applications · 2015Article
- Cdk1 promotes cytokinesis in fission yeast through activation of the septation initiation network.Molecular biology of the cell · 2014Article
- Cdc5-dependent asymmetric localization of bfa1 fine-tunes timely mitotic exit.PLoS genetics · 2012Article
- Tem1 localization to the spindle pole bodies is essential for mitotic exit and impairs spindle checkpoint function.The Journal of cell biology · 2011Article
- Monitoring spindle orientation: Spindle position checkpoint in charge.Cell division · 2010Article
- Lte1 contributes to Bfa1 localization rather than stimulating nucleotide exchange by Tem1.The Journal of cell biology · 2009Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In budding yeast, Tem1 is a key regulator of mitotic exit. Bfa1/Bub2 stimulates Tem1 GTPase activity as a GTPase-activating protein (GAP). Lte1 possesses a guanine-nucleotide exchange factor (GEF) domain likely for Tem1. However, recent observations showed that cells may control mitotic exit without either Lte1 or Bfa1/Bub2 GAP activity, obscuring how Tem1 is regulated. Here, we assayed BFA1 mutants with varying GAP activities for Tem1, showing for the first time that Bfa1/Bub2 GAP activity inhibits Tem1 in vivo. A decrease in GAP activity allowed cells to bypass mitotic exit defects. Interestingly, different levels of GAP activity were required to prevent mitotic exit depending on the type of perturbation. Although essential, more Bfa1/Bub2 GAP activity was needed for spindle damage than for DNA damage to fully activate the checkpoint. Conversely, Bfa1/Bub2 GAP activity was insufficient to delay mitotic exit in cells with misoriented spindles. Instead, decreased interaction of Bfa1 with Kin4 was observed in BFA1 mutant cells with a defective spindle position checkpoint. These findings demonstrate that there is a GAP-independent surveillance mechanism of Bfa1/Bub2, which, together with the GTP/GDP switch of Tem1, may be required for the genomic stability of cells with misaligned spindles.
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