ArticleMolecular genetics and genomics : MGG2003
Mutations in the yeast cyclin-dependent kinase Cdc28 reveal a role in the spindle assembly checkpoint.
Article in Molecular genetics and genomics : MGG, 2003. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 19 citations in OpenAlex.
- Post-translational Regulation of DNA Polymerase η, a Connection to Damage-Induced Cohesion inGenetics · 2020Article
- Recent advances in understanding the role of Cdk1 in the Spindle Assembly Checkpoint.F1000Research · 2020Review
- Adaptation to the spindle checkpoint is regulated by the interplay between Cdc28/Clbs and PP2ACdc55.The Journal of cell biology · 2013Article
- Natural variation in CDC28 underlies morphological phenotypes in an environmental yeast isolate.Genetics · 2011Article
- The RSC chromatin-remodeling complex influences mitotic exit and adaptation to the spindle assembly checkpoint by controlling the Cdc14 phosphatase.The Journal of cell biology · 2010Article
- An overview of Cdk1-controlled targets and processes.Cell division · 2010Article
- Overcoming inhibition in the spindle checkpoint.Genes & development · 2009Review
- A phosphorylation-independent role for the yeast cyclin-dependent kinase activating kinase Cak1.Gene · 2009Article
- Cdc28/Cdk1 positively and negatively affects genome stability in S. cerevisiae.The Journal of cell biology · 2009Article
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- Distinct sequence elements of cyclin B1 promote localization to chromatin, centrosomes, and kinetochores during mitosis.Molecular biology of the cell · 2007Article
- Budesonide exerts its chemopreventive efficacy during mouse lung tumorigenesis by modulating gene expressions.Oncogene · 2004Article
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Anaphase onset and mitotic exit are regulated by the spindle assembly or kinetochore checkpoint, which inhibits the anaphase-promoting complex (APC), preventing the degradation of anaphase inhibitors and mitotic cyclins. As a result, cells arrest with high cyclin-dependent kinase (CDK) activity due to the accumulation of cyclins. Aside from this, a clear-cut demonstration of a direct role for CDKs in the spindle checkpoint response has been elusive. Cdc28 is the main CDK driving the cell cycle in budding yeast. In this report, mutations in cdc28 are described that confer specific checkpoint defects, supersensitivity towards microtubule poisons and chromosome loss. Two alleles encode single mutations in the N and C terminal regions, respectively (R10G and R288G), and one allele specifies two mutations near the C terminus (F245L, I284T). These cdc28 mutants are unable to arrest or efficiently prevent sister chromatid separation during treatment with nocodazole. Genetic interactions with checkpoint and apc mutants suggest Cdc28 may regulate checkpoint arrest downstream of the MAD2 and BUB2 pathways. These studies identify a C-terminal domain of Cdc28 required for checkpoint arrest upon spindle damage that mediates chromosome stability during vegetative growth, suggesting that it has an essential surveillance function in the unperturbed cell cycle.
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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.