ArticleMolecular and cellular biology2005
Cooperative control of Crb2 by ATM family and Cdc2 kinases is essential for the DNA damage checkpoint in fission yeast.
Article in Molecular and cellular biology, 2005. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 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
16 citing papers in PubMed, 27 citations in OpenAlex.
- Pot1 promotes telomere DNA replication via the Stn1-Ten1 complex in fission yeast.Nucleic acids research · 2023Article
- Review
- Article
- Identification of novel genes involved in DNA damage response by screening a genome-wide Schizosaccharomyces pombe deletion library.BMC genomics · 2012Article
- Multiple phosphorylation of Rad9 by CDK is required for DNA damage checkpoint activation.Cell cycle (Georgetown, Tex.) · 2012Article
- Dual recruitment of Cdc48 (p97)-Ufd1-Npl4 ubiquitin-selective segregase by small ubiquitin-like modifier protein (SUMO) and ubiquitin in SUMO-targeted ubiquitin ligase-mediated genome stability functions.The Journal of biological chemistry · 2012Article
- Bat3 facilitates H3K79 dimethylation by DOT1L and promotes DNA damage-induced 53BP1 foci at G1/G2 cell-cycle phases.The EMBO journal · 2012Article
- Eukaryotic DNA damage checkpoint activation in response to double-strand breaks.Cellular and molecular life sciences : CMLS · 2012Review
- Regulatory networks integrating cell cycle control with DNA damage checkpoints and double-strand break repair.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2011Review
- BRCT domain interactions with phospho-histone H2A target Crb2 to chromatin at double-strand breaks and maintain the DNA damage checkpoint.Molecular and cellular biology · 2010Article
- Requirement for the phospho-H2AX binding module of Crb2 in double-strand break targeting and checkpoint activation.Molecular and cellular biology · 2010Article
- Epigenetic modifications in double-strand break DNA damage signaling and repair.Clinical cancer research : an official journal of the American Association for Cancer Research · 2010Review
- Di-methyl H4 lysine 20 targets the checkpoint protein Crb2 to sites of DNA damage.The Journal of biological chemistry · 2008Article
- Structural and functional analysis of the Crb2-BRCT2 domain reveals distinct roles in checkpoint signaling and DNA damage repair.Genes & development · 2008Article
- Article
- Histone modification-dependent and -independent pathways for recruitment of checkpoint protein Crb2 to double-strand breaks.Genes & development · 2006Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
Abstract
The cellular responses to double-stranded breaks (DSBs) typically involve the extensive accumulation of checkpoint proteins in chromatin surrounding the damaged DNA. One well-characterized example involves the checkpoint protein Crb2 in the fission yeast Schizosaccharomyces pombe. The accumulation of Crb2 at DSBs requires the C-terminal phosphorylation of histone H2A (known as gamma-H2A) by ATM family kinases in chromatin surrounding the break. It also requires the constitutive methylation of histone H4 on lysine-20 (K20). Interestingly, neither type of histone modification is essential for the Crb2-dependent checkpoint response. However, H4-K20 methylation is essential in a crb2-T215A strain that lacks a cyclin-dependent kinase phosphorylation site in Crb2. Here we explain this genetic interaction by describing a previously overlooked effect of the crb2-T215A mutation. We show that crb2-T215A cells are able to initiate but not sustain a checkpoint response. We also report that gamma-H2A is essential for the DNA damage checkpoint in crb2-T215A cells. Importantly, we show that inactivation of Cdc2 in gamma-H2A-defective cells impairs Crb2-dependent signaling to the checkpoint kinase Chk1. These findings demonstrate that full Crb2 activity requires phosphorylation of threonine-215 by Cdc2. This regulation of Crb2 is independent of the histone modifications that are required for the hyperaccumulation of Crb2 at DSBs.
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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.