Dynamics of Rad9 Chromatin Binding and Checkpoint Function Are Mediated by Its Dimerization and Are Cell Cycle–Regulated by CDK1 Activity
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Summary
In G1 cells, GST or FKBP dimerization motifs can substitute to the BRCT domains for Rad9 chromatin binding and checkpoint function, and forced Rad9 diming in M phase fails to promote its recruitment onto DNA, although it supports Rad9 checkpoint function.
- Type
- article
- Published
- 2010-08-01
- Cited by
- 79
- References
- 77
- Access
- Open access
- OpenAlex
- https://openalex.org/W1963889969
- Semantic Scholar
- https://api.semanticscholar.org/CorpusID:18303268
Keywords
G2-M DNA damage checkpoint, Chromatin, Cell biology, Cell cycle checkpoint, Biology
References
- Ste5 RING-H2 domain: role in Ste4-promoted oligomerization for yeast pheromone signaling.
- The budding yeast Rad9 checkpoint protein is subjected to Mec1/Tel1‐dependent hyperphosphorylation and interacts with Rad53 after DNA damage
- Structural basis for the methylation state-specific recognition of histone H4-K20 by 53BP1 and Crb2 in DNA repair.
- In vivo site-directed mutagenesis using oligonucleotides
- Docking onto chromatin via the Saccharomyces cerevisiae Rad9 Tudor domain
- A role for Saccharomyces cerevisiae histone H2A in DNA repair
- A chemical switch for inhibitor-sensitive alleles of any protein kinase
- The checkpoint protein Ddc2, functionally related to S. pombe Rad26, interacts with Mec1 and is regulated by Mec1-dependent phosphorylation in budding yeast.
- MEC1-dependent phosphorylation of Rad9p in response to DNA damage.
- Additional modules for versatile and economical PCR‐based gene deletion and modification in Saccharomyces cerevisiae
- De novo synthesis of budding yeast DNA polymerase α and POLI transcription at the G1/S boundary are not required for entrance into S phase
- Orchestration of the DNA-damage response by the RNF8 ubiquitin ligase
- The Tandem BRCT Domain of 53BP1 Is Not Required for Its Repair Function*
- RNF8 ubiquitylates histones at DNA double-strand breaks and promotes assembly of repair proteins.
- Characterization of the activation domain of the Rad53 checkpoint kinase
- The CDK regulates repair of double‐strand breaks by homologous recombination during the cell cycle
- Maintenance of the DNA-Damage Checkpoint Requires DNA-Damage-Induced Mediator Protein Oligomerization
- The RAD9 gene controls the cell cycle response to DNA damage in Saccharomyces cerevisiae.
- Homo-oligomerization Is the Essential Function of the Tandem BRCT Domains in the Checkpoint Protein Crb2*
- DNA end resection, homologous recombination and DNA damage checkpoint activation require CDK1
Cited by
- Sensing of Replication Stress and Mec1 Activation Act through Two Independent Pathways Involving the 9-1-1 Complex and DNA Polymerase ε
- Mec1/ATR regulates the generation of single‐stranded DNA that attenuates Tel1/ATM signaling at DNA ends
- Chromatin Regulators and DNA Repair: A Dissertation
- Dimerization Mediated by a Divergent Forkhead-associated Domain Is Essential for the DNA Damage and Spindle Functions of Fission Yeast Mdb1.
- Dpb11 coordinates Mec1 kinase activation with cell cycle-regulated Rad9 recruitment
- Functional Interplay between the 53BP1-Ortholog Rad9 and the Mre11 Complex Regulates Resection, End-Tethering and Repair of a Double-Strand Break
- Cell cycle regulation of DNA double-strand break end resection by Cdk1-dependent Dna2 phosphorylation
- Eukaryotic DNA damage checkpoint activation in response to double-strand breaks
- The DNA damage response during mitosis.
- Rad9 interacts with Aft1 to facilitate genome surveillance in fragile genomic sites under non-DNA damage-inducing conditions in S. cerevisiae
- Initiation of chromosomal DNA replication in eukaryotic cells; contribution of yeast genetics to the elucidation.
- Multiple phosphorylation of Rad9 by CDK is required for DNA damage checkpoint activation
- DNA Repair Scaffolds Dampen Checkpoint Signaling by Counteracting the Rad9 Adaptor
- The many roads to checkpoint activation
- To trim or not to trim: Progression and control of DSB end resection
- Regulation of the DNA damage response by cyclin-dependent kinases.
- Interplays between ATM/Tel1 and ATR/Mec1 in sensing and signaling DNA double-strand breaks.
- Chemical Genetics: Budding Yeast as a Platform for Drug Discovery and Mapping of Genetic Pathways
- Ddc2 Mediates Mec1 Activation through a Ddc1- or Dpb11-Independent Mechanism
- Site-Specific Phosphorylation of the DNA Damage Response Mediator Rad9 by Cyclin-Dependent Kinases Regulates Activation of Checkpoint Kinase 1
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