ArticleDNA repair2013
DNA resection proteins Sgs1 and Exo1 are required for G1 checkpoint activation in budding yeast.
Article in DNA repair, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- Checkpoint phosphorylation sites on budding yeast Rif1 protect nascent DNA from degradation by Sgs1-Dna2.PLoS genetics · 2023Article
- Article
- RecQ DNA Helicase Rqh1 Promotes Rad3Molecular and cellular biology · 2020Article
- Quantitative mechanisms of DNA damage sensing and signaling.Current genetics · 2020Review
- Measuring Single-Cell Phenotypic Growth Heterogeneity Using a Microfluidic Cell Volume Sensor.Scientific reports · 2018Article
- A novel method of using Deep Belief Networks and genetic perturbation data to search for yeast signaling pathways.PloS one · 2018Article
- A meeting at risk: Unrepaired DSBs go for broke.Nucleus (Austin, Tex.) · 2017Review
- Fidelity of end joining in mammalian episomes and the impact of Metnase on joint processing.BMC molecular biology · 2014Article
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
Double-strand breaks (DSBs) in budding yeast trigger activation of DNA damage checkpoints, allowing repair to occur. Although resection is necessary for initiating damage-induced cell cycle arrest in G2, no role has been assigned to it in the activation of G1 checkpoint. Here we demonstrate for the first time that the resection proteins Sgs1 and Exo1 are required for efficient G1 checkpoint activation. We find in G1 arrested cells that histone H2A phosphorylation in response to ionizing radiation is independent of Sgs1 and Exo1. In contrast, these proteins are required for damage-induced recruitment of Rfa1 to the DSB sites, phosphorylation of the Rad53 effector kinase, cell cycle arrest and RNR3 expression. Checkpoint activation in G1 requires the catalytic activity of Sgs1, suggesting that it is DNA resection mediated by Sgs1 that stimulates the damage response pathway rather than protein-protein interactions with other DDR proteins. Together, these results implicate DNA resection, which is thought to be minimal in G1, as necessary for activation of the G1 checkpoint.
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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.