Details
- Autor(en) / Beteiligte
- Titel
- DNA end resection by CtIP and exonuclease 1 prevents genomic instability
- Ist Teil von
- EMBO reports, 2010-12, Vol.11 (12), p.962-968
- Ort / Verlag
- Chichester, UK: John Wiley & Sons, Ltd
- Erscheinungsjahr
- 2010
- Link zum Volltext
- Quelle
- Free E-Journal (出版社公開部分のみ）
- Beschreibungen/Notizen
- End resection of DNA—which is essential for the repair of DNA double‐strand breaks (DSBs) by homologous recombination—relies first on the partnership between MRE11–RAD50–NBS1 (MRN) and CtIP, followed by a processive step involving helicases and exonucleases such as exonuclease 1 (EXO1). In this study, we show that the localization of EXO1 to DSBs depends on both CtIP and MRN. We also establish that CtIP interacts with EXO1 and restrains its exonucleolytic activity in vitro. Finally, we show that on exposure to camptothecin, depletion of EXO1 in CtIP‐deficient cells increases the frequency of DNA–PK‐dependent radial chromosome formation. Thus, our study identifies new functions of CtIP and EXO1 in DNA end resection and provides new information on the regulation of DSB repair pathways, which is a key factor in the maintenance of genome integrity. This study reports on the collaborative action of human CtIP and EXO1 in DNA end resection during DNA double‐strand break repair to prevent the formation of abnormal chromosome structures.
- Sprache
- Englisch
- Identifikatoren
- ISSN: 1469-221XeISSN: 1469-3178DOI: 10.1038/embor.2010.157Titel-ID: cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_2999859
- Format
- –
- Schlagworte
- camptothecin, Carrier Proteins - metabolism, Cell Line, Tumor, CtIP, Cytoprotection, DNA Breaks, Double-Stranded, DNA damage, DNA double-strand break repair, DNA Repair, DNA Repair Enzymes - metabolism, DNA-Activated Protein Kinase - metabolism, DNA-Binding Proteins - metabolism, Exodeoxyribonucleases - metabolism, exonuclease 1, Genomic Instability, Genomics, HEK293 Cells, Humans, Molecular biology, MRE11 Homologue Protein, Nuclear Proteins - metabolism, Protein Binding, Proteins, Recombination, Genetic - genetics, Scientific Reports