ArticleThe Journal of biological chemistry2013
Defective in mitotic arrest 1 (Dma1) ubiquitin ligase controls G1 cyclin degradation.
Article in The Journal of biological chemistry, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed, 9 citations in OpenAlex.
- A comprehensive, mechanistically detailed, and executable model of the cell division cycle in Saccharomyces cerevisiae.Nature communications · 2019Article
- Redundancy or specificity? The role of the CDK Pho85 in cell cycle control.International journal of biochemistry and molecular biology · 2013Review
- Phosphate-activated cyclin-dependent kinase stabilizes G1 cyclin to trigger cell cycle entry.Molecular and cellular biology · 2013Article
- Catalysis-dependent and redundant roles of Dma1 and Dma2 in maintenance of genome stability in Saccharomyces cerevisiae.The Journal of biological chemistryArticle
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Progression through the G(1) phase of the cell cycle is controlled by diverse cyclin-dependent kinases (CDKs) that might be associated to numerous cyclin isoforms. Given such complexity, regulation of cyclin degradation should be crucial for coordinating progression through the cell cycle. In Saccharomyces cerevisiae, SCF is the only E3 ligase known to date to be involved in G(1) cyclin degradation. Here, we report the design of a genetic screening that uncovered Dma1 as another E3 ligase that targets G(1) cyclins in yeast. We show that the cyclin Pcl1 is ubiquitinated in vitro and in vivo by Dma1, and accordingly, is stabilized in dma1 mutants. We demonstrate that Pcl1 must be phosphorylated by its own CDK to efficiently interact with Dma1 and undergo degradation. A nonphosphorylatable version of Pcl1 accumulates throughout the cell cycle, demonstrating the physiological relevance of the proposed mechanism. Finally, we present evidence that the levels of Pcl1 and Cln2 are independently controlled in response to nutrient availability. This new previously unknown mechanism for G(1) cyclin degradation that we report here could help elucidate the specific roles of the redundant CDK-cyclin complexes in G(1).
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Registered trials
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