ArticlePLoS genetics2022
Repression of essential cell cycle genes increases cellular fitness.
Article in PLoS genetics, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 8 citations in OpenAlex.
- Molecular evolution in light of regulatory-coding epistasis.EMBO reports · 2026Review
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- rDNA copy number variation affects yeast fitness in response to different environments.Genetics · 2025Article
- Vacuolar protein sorting-associated protein Vps17 regulates sexual reproduction and virulence ofMycology · 2025Article
- Calcineurin promotes adaptation to chronic stress through two distinct mechanisms.Molecular biology of the cell · 2024Article
- Revealing the Mechanism of Aroma Production Driven by High Salt Stress inFoods (Basel, Switzerland) · 2024Article
- Calcineurin promotes adaptation to chronic stress through two distinct mechanisms.bioRxiv : the preprint server for biology · 2024Article
- Phosphosite Scanning reveals a complex phosphorylation code underlying CDK-dependent activation of Hcm1.Nature communications · 2023Article
Corrections and comments
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Authors and funding
12 authors at 3 institutions in 2 countries.
Funding
Abstract
A network of transcription factors (TFs) coordinates transcription with cell cycle events in eukaryotes. Most TFs in the network are phosphorylated by cyclin-dependent kinase (CDK), which limits their activities during the cell cycle. Here, we investigate the physiological consequences of disrupting CDK regulation of the paralogous repressors Yhp1 and Yox1 in yeast. Blocking Yhp1/Yox1 phosphorylation increases their levels and decreases expression of essential cell cycle regulatory genes which, unexpectedly, increases cellular fitness in optimal growth conditions. Using synthetic genetic interaction screens, we find that Yhp1/Yox1 mutations improve the fitness of mutants with mitotic defects, including condensin mutants. Blocking Yhp1/Yox1 phosphorylation simultaneously accelerates the G1/S transition and delays mitotic exit, without decreasing proliferation rate. This mitotic delay partially reverses the chromosome segregation defect of condensin mutants, potentially explaining their increased fitness when combined with Yhp1/Yox1 phosphomutants. These findings reveal how altering expression of cell cycle genes leads to a redistribution of cell cycle timing and confers a fitness advantage to cells.
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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.