ArticleGenetics2002
Precocious S-phase entry in budding yeast prolongs replicative state and increases dependence upon Rad53 for viability.
Article in Genetics, 2002. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
17 citing papers in PubMed, 31 citations in OpenAlex.
- Article
- Whi7/Srl3 polymorphisms reveal its role in cell size and quiescence.microPublication biology · 2022Article
- Checkpoint inhibition of origin firing prevents inappropriate replication outside of S-phase.eLife · 2021Article
- A common strategy for initiating the transition from proliferation to quiescence.Current genetics · 2017Review
- Characterization of dependencies between growth and division in budding yeast.Journal of the Royal Society, Interface · 2017Article
- Msa1 and Msa2 Modulate G1-Specific Transcription to Promote G1 Arrest and the Transition to Quiescence in Budding Yeast.PLoS genetics · 2016Article
- ZD7288, a blocker of the HCN channel family, increases doubling time of mouse embryonic stem cells and modulates differentiation outcomes in a context-dependent manner.SpringerPlus · 2016Article
- Xbp1 directs global repression of budding yeast transcription during the transition to quiescence and is important for the longevity and reversibility of the quiescent state.PLoS genetics · 2013Article
- End-of-life cell cycle arrest contributes to stochasticity of yeast replicative aging.FEMS yeast research · 2013Article
- Cell cycle regulation of DNA replication.Annual review of genetics · 2007Review
- Novel role for checkpoint Rad53 protein kinase in the initiation of chromosomal DNA replication in Saccharomyces cerevisiae.Genetics · 2006Article
- The F-box protein Dia2 regulates DNA replication.Molecular biology of the cell · 2006Article
- Article
- Article
- Diabetes and exocrine pancreatic insufficiency in E2F1/E2F2 double-mutant mice.The Journal of clinical investigation · 2004Article
- Defective gene expression, S phase progression, and maturation during hematopoiesis in E2F1/E2F2 mutant mice.Molecular and cellular biology · 2003Article
- Rad53 checkpoint kinase phosphorylation site preference identified in the Swi6 protein of Saccharomyces cerevisiae.Molecular and cellular biology · 2003Article
Corrections and comments
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Precocious entry into S phase due to overproduction of G1 regulators can cause genomic instability. The mechanisms of this phenomenon are largely unknown. We explored the consequences of precocious S phase in yeast by overproducing a deregulated form of Swi4 (Swi4-t). Swi4 is a late G1-specific transcriptional activator that, in complex with Swi6, binds to SCB elements and activates late G1-specific genes, including G1 cyclins. We find that wild-type cells tolerate Swi4-t, whereas checkpoint-deficient rad53-11 cells lose viability within several divisions when Swi4-t is overproduced. Rad53 kinase activity is increased in cells overproducing Swi4-t, indicating activation of the checkpoint. We monitored the transition from G1 to S in cells with Swi4-t and found that there is precocious S-phase entry and that the length of S phase is extended. Moreover, there were more replication intermediates, and firing of at least a subset of origins may have been more extensive in the cells expressing Swi4-t. Our working hypothesis is that Rad53 modulates origin firing based upon growth conditions to optimize the rate of S-phase progression without adversely affecting fidelity. This regulation becomes essential when S phase is influenced by Swi4-t.
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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.