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Article: RAD18 transmits DNA damage signalling to elicit homologous recombination repair
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TitleRAD18 transmits DNA damage signalling to elicit homologous recombination repair
 
AuthorsHuang, J3
Huen, MSY3
Kim, H3 4
Leung, CCY2
Glover, JNM2
Yu, X1
Chen, J3
 
KeywordsChemicals And Cas Registry Numbers
 
Issue Date2009
 
PublisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/naturecellbiology
 
CitationNature Cell Biology, 2009, v. 11 n. 5, p. 592-603 [How to Cite?]
DOI: http://dx.doi.org/10.1038/ncb1865
 
AbstractTo maintain genome stability, cells respond to DNA damage by activating signalling pathways that govern cell-cycle checkpoints and initiate DNA repair. Cell-cycle checkpoint controls should connect with DNA repair processes, however, exactly how such coordination occurs in vivo is largely unknown. Here we describe a new role for the E3 ligase RAD18 as the integral component in translating the damage response signal to orchestrate homologous recombination repair (HRR). We show that RAD18 promotes homologous recombination in a manner strictly dependent on its ability to be recruited to sites of DNA breaks and that this recruitment relies on a well-defined DNA damage signalling pathway mediated by another E3 ligase, RNF8. We further demonstrate that RAD18 functions as an adaptor to facilitate homologous recombination through direct interaction with the recombinase RAD51C. Together, our data uncovers RAD18 as a key factor that orchestrates HRR through surveillance of the DNA damage signal.
 
ISSN1465-7392
2013 Impact Factor: 20.058
 
DOIhttp://dx.doi.org/10.1038/ncb1865
 
PubMed Central IDPMC2743127
 
ISI Accession Number IDWOS:000265640000018
Funding AgencyGrant Number
National Institutes of Health
Anna Fuller Fund Fellowship
Department of Defense
Funding Information:

We thank T. Shiomi for HCT116 RAD18-/- cells, M. Yamaizumi for RAD18-/- MEFs, S. Akira for UBC13-deficient cells, H. Nagasawa for IRS3 and V79 cells, M. Jasin for U2OS cells with DR-GFP integration and pCBASce plasmids, B. P. Chen for NU7441 and J. Groenendyk for helping with the BIAcore system. J. C would like to thank all colleagues for discussions and technical assistance, and J. Wood for proofreading. This work was supported by grants from the National Institutes of Health to J. C., M. S. Y. H. is supported by the Anna Fuller Fund Fellowship and J. C. is a recipient of an Era of Hope Scholar award from the Department of Defense ( a member of the Mayo Clinic Breast SPORE program).

 
ReferencesReferences in Scopus
 
DC FieldValue
dc.contributor.authorHuang, J
 
dc.contributor.authorHuen, MSY
 
dc.contributor.authorKim, H
 
dc.contributor.authorLeung, CCY
 
dc.contributor.authorGlover, JNM
 
dc.contributor.authorYu, X
 
dc.contributor.authorChen, J
 
dc.date.accessioned2010-09-17T10:09:36Z
 
dc.date.available2010-09-17T10:09:36Z
 
dc.date.issued2009
 
dc.description.abstractTo maintain genome stability, cells respond to DNA damage by activating signalling pathways that govern cell-cycle checkpoints and initiate DNA repair. Cell-cycle checkpoint controls should connect with DNA repair processes, however, exactly how such coordination occurs in vivo is largely unknown. Here we describe a new role for the E3 ligase RAD18 as the integral component in translating the damage response signal to orchestrate homologous recombination repair (HRR). We show that RAD18 promotes homologous recombination in a manner strictly dependent on its ability to be recruited to sites of DNA breaks and that this recruitment relies on a well-defined DNA damage signalling pathway mediated by another E3 ligase, RNF8. We further demonstrate that RAD18 functions as an adaptor to facilitate homologous recombination through direct interaction with the recombinase RAD51C. Together, our data uncovers RAD18 as a key factor that orchestrates HRR through surveillance of the DNA damage signal.
 
dc.description.naturelink_to_subscribed_fulltext
 
dc.identifier.citationNature Cell Biology, 2009, v. 11 n. 5, p. 592-603 [How to Cite?]
DOI: http://dx.doi.org/10.1038/ncb1865
 
dc.identifier.citeulike4448001
 
dc.identifier.doihttp://dx.doi.org/10.1038/ncb1865
 
dc.identifier.epage603
 
dc.identifier.f10001160460
 
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dc.identifier.f10001160460
 
dc.identifier.f10001160460
 
dc.identifier.f10001160460
 
dc.identifier.f10001160460
 
dc.identifier.isiWOS:000265640000018
Funding AgencyGrant Number
National Institutes of Health
Anna Fuller Fund Fellowship
Department of Defense
Funding Information:

We thank T. Shiomi for HCT116 RAD18-/- cells, M. Yamaizumi for RAD18-/- MEFs, S. Akira for UBC13-deficient cells, H. Nagasawa for IRS3 and V79 cells, M. Jasin for U2OS cells with DR-GFP integration and pCBASce plasmids, B. P. Chen for NU7441 and J. Groenendyk for helping with the BIAcore system. J. C would like to thank all colleagues for discussions and technical assistance, and J. Wood for proofreading. This work was supported by grants from the National Institutes of Health to J. C., M. S. Y. H. is supported by the Anna Fuller Fund Fellowship and J. C. is a recipient of an Era of Hope Scholar award from the Department of Defense ( a member of the Mayo Clinic Breast SPORE program).

 
dc.identifier.issn1465-7392
2013 Impact Factor: 20.058
 
dc.identifier.issue5
 
dc.identifier.pmcidPMC2743127
 
dc.identifier.pmid19396164
 
dc.identifier.scopuseid_2-s2.0-67349168142
 
dc.identifier.spage592
 
dc.identifier.urihttp://hdl.handle.net/10722/90869
 
dc.identifier.volume11
 
dc.languageeng
 
dc.publisherNature Publishing Group. The Journal's web site is located at http://www.nature.com/naturecellbiology
 
dc.publisher.placeUnited Kingdom
 
dc.relation.ispartofNature Cell Biology
 
dc.relation.referencesReferences in Scopus
 
dc.subjectChemicals And Cas Registry Numbers
 
dc.titleRAD18 transmits DNA damage signalling to elicit homologous recombination repair
 
dc.typeArticle
 
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Author Affiliations
  1. University of Michigan Medical School
  2. University of Alberta
  3. Yale University School of Medicine
  4. Sungkyunkwan University