Document Detail


Srs2 plays a critical role in reversible G2 arrest upon chronic and low doses of UV irradiation via two distinct homologous recombination-dependent mechanisms in postreplication repair-deficient cells.
MedLine Citation:
PMID:  20713444     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
Differential posttranslational modification of proliferating cell nuclear antigen (PCNA) by ubiquitin or SUMO plays an important role in coordinating the processes of DNA replication and DNA damage tolerance. Previously it was shown that the loss of RAD6-dependent error-free postreplication repair (PRR) results in DNA damage checkpoint-mediated G(2) arrest in cells exposed to chronic low-dose UV radiation (CLUV), whereas wild-type and nucleotide excision repair-deficient cells are largely unaffected. In this study, we report that suppression of homologous recombination (HR) in PRR-deficient cells by Srs2 and PCNA sumoylation is required for checkpoint activation and checkpoint maintenance during CLUV irradiation. Cyclin-dependent kinase (CDK1)-dependent phosphorylation of Srs2 did not influence checkpoint-mediated G(2) arrest or maintenance in PRR-deficient cells but was critical for HR-dependent checkpoint recovery following release from CLUV exposure. These results indicate that Srs2 plays an important role in checkpoint-mediated reversible G(2) arrest in PRR-deficient cells via two separate HR-dependent mechanisms. The first (required to suppress HR during PRR) is regulated by PCNA sumoylation, whereas the second (required for HR-dependent recovery following CLUV exposure) is regulated by CDK1-dependent phosphorylation.
Authors:
Takashi Hishida; Yoshihiro Hirade; Nami Haruta; Yoshino Kubota; Hiroshi Iwasaki
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't     Date:  2010-08-16
Journal Detail:
Title:  Molecular and cellular biology     Volume:  30     ISSN:  1098-5549     ISO Abbreviation:  Mol. Cell. Biol.     Publication Date:  2010 Oct 
Date Detail:
Created Date:  2010-09-23     Completed Date:  2010-10-28     Revised Date:  2013-05-29    
Medline Journal Info:
Nlm Unique ID:  8109087     Medline TA:  Mol Cell Biol     Country:  United States    
Other Details:
Languages:  eng     Pagination:  4840-50     Citation Subset:  IM    
Affiliation:
Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan. hishida@biken.osaka-u.ac.jp
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MeSH Terms
Descriptor/Qualifier:
Antigens, Nuclear / genetics,  metabolism
CDC2 Protein Kinase / metabolism
DNA Helicases / genetics,  metabolism*
DNA Repair
DNA Replication
DNA, Fungal / genetics,  metabolism
DNA, Single-Stranded / genetics,  metabolism
DNA-Binding Proteins / genetics,  metabolism
G2 Phase / radiation effects
Gene Deletion
Genes, Fungal
Models, Biological
Mutation
Phosphorylation
Proliferating Cell Nuclear Antigen / metabolism
Radiation Tolerance / genetics,  physiology
Recombination, Genetic
Saccharomyces cerevisiae / cytology,  genetics,  metabolism*,  radiation effects
Saccharomyces cerevisiae Proteins / genetics,  metabolism*
Small Ubiquitin-Related Modifier Proteins / metabolism
Ultraviolet Rays
Chemical
Reg. No./Substance:
0/Antigens, Nuclear; 0/DNA, Fungal; 0/DNA, Single-Stranded; 0/DNA-Binding Proteins; 0/POL30 protein, S cerevisiae; 0/Proliferating Cell Nuclear Antigen; 0/RAD18 protein, S cerevisiae; 0/Saccharomyces cerevisiae Proteins; 0/Small Ubiquitin-Related Modifier Proteins; 125481-05-2/HPR5 protein, S cerevisiae; EC 2.7.11.22/CDC2 Protein Kinase; EC 3.6.1.-/DNA Helicases
Comments/Corrections

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