ArticleProceedings of the National Academy of Sciences of the United States of America2022
Cip1 tunes cell cycle arrest duration upon calcineurin activation.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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Who cites it
5 citing papers in PubMed, 7 citations in OpenAlex.
- Dynamic phosphorylation of Hcm1 promotes fitness in chronic stress.PLoS genetics · 2025Article
- Dynamic phosphorylation of Hcm1 promotes fitness in chronic stress.bioRxiv : the preprint server for biology · 2025Article
- Dual regulation of the levels and function of Start transcriptional repressors drives G1 arrest in response to cell wall stress.Cell communication and signaling : CCS · 2025Article
- Calcineurin promotes adaptation to chronic stress through two distinct mechanisms.Molecular biology of the cell · 2024Article
- Calcineurin promotes adaptation to chronic stress through two distinct mechanisms.bioRxiv : the preprint server for biology · 2024Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Cells exposed to environmental stress arrest the cell cycle until they have adapted to their new environment. Cells adjust the length of the arrest for each unique stressor, but how they do this is not known. Here, we investigate the role of the stress-activated phosphatase calcineurin (CN) in controlling cell cycle arrest in Saccharomyces cerevisiae. We find that CN controls arrest duration through activation of the G1 cyclin–dependent kinase inhibitor Cip1. Our results demonstrate that multiple stressors trigger a G1/S arrest through Hog1-dependent down-regulation of G1 cyclin transcription. When a stressor also activates CN, this arrest is lengthened as CN prolongs Hog1-dependent phosphorylation of Cip1. Cip1 plays no role in response to stressors that activate Hog1 but not CN. These findings illustrate how stress response pathways cooperate to tailor the stress response and suggest that Cip1 functions to prolong cell cycle arrest when a cell requires additional time for adaptation.
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Registered trials
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