ArticleG3 (Bethesda, Md.)2020
Checkpoint Regulation of Nuclear Tos4 Defines S Phase Arrest in Fission Yeast.
Article in G3 (Bethesda, Md.), 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed.
- Hydroxyurea induces an oxidative stress response that triggers ER expansion and cytoplasmic protein aggregation.PLoS biology · 2025Article
- Genetic-interaction screens uncover novel biological roles and regulators of transcription factors in fission yeast.G3 (Bethesda, Md.) · 2022Article
- Determinants of RPA megafoci localization to the nuclear periphery in response to replication stress.G3 (Bethesda, Md.) · 2022Article
- Photo Phenosizer, a rapid machine learning-based method to measure cell dimensions in fission yeast.microPublication biology · 2022Article
- Novel Antifungal Activity of Q-Griffithsin, a Broad-Spectrum Antiviral Lectin.Microbiology spectrum · 2021Article
- A visual atlas of meiotic protein dynamics in living fission yeast.Open biology · 2021Article
- Active Replication Checkpoint Drives Genome Instability in Fission YeastMolecular and cellular biology · 2020Article
Corrections and comments
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Authors and funding
4 authors.
Funding
Abstract
From yeast to humans, the cell cycle is tightly controlled by regulatory networks that regulate cell proliferation and can be monitored by dynamic visual markers in living cells. We have observed S phase progression by monitoring nuclear accumulation of the FHA-containing DNA binding protein Tos4, which is expressed in the G1/S phase transition. We use Tos4 localization to distinguish three classes of DNA replication mutants: those that arrest with an apparent 1C DNA content and accumulate Tos4 at the restrictive temperature; those that arrest with an apparent 2C DNA content, that do not accumulate Tos4; and those that proceed into mitosis despite a 1C DNA content, again without Tos4 accumulation. Our data indicate that Tos4 localization in these conditions is responsive to checkpoint kinases, with activation of the Cds1 checkpoint kinase promoting Tos4 retention in the nucleus, and activation of the Chk1 damage checkpoint promoting its turnover. Tos4 localization therefore allows us to monitor checkpoint-dependent activation that responds to replication failure in early
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