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Bachl, J. ; Ertongur, I. ; Jungnickel, B.

Involvement of Rad18 in somatic hypermutation.

Proc. Natl. Acad. Sci. U.S.A. 103, 12081-12086 (2006)
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Somatic hypermutation of Ig genes is initiated by transcription-coupled cytidine deamination in Ig loci. Error-prone processing of the resultant DNA lesions is thought to cause extensive mutagenesis, but it is presently an enigma how and why error-prone rather than error-free repair pathways are recruited. During DNA replication, recruitment of error-prone translesion polymerases may be mediated by Rad6/Rad18-mediated ubiquitination of proliferating cell nuclear antigen, a major switchboard controlling the fidelity of DNA lesion bypass in eukaryotes. By inactivation of Rad18 in the DT40 B cell line, we show that the Rad6 pathway is involved in somatic hypermutation in these cells. Our findings imply that targeted recruitment of mutagenic polymerases by the Rad6 pathway contributes to the complex process of somatic hypermutation and provide a framework for more detailed mechanistic studies of the mutagenesis phase of secondary Ig diversification.
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Publikationstyp Artikel: Journalartikel
Dokumenttyp Wissenschaftlicher Artikel
Schlagwörter proliferating cell nuclear antigen; ubiquitination; Rad6 pathway; IMMUNOGLOBULIN GENE CONVERSION; DNA-POLYMERASE-ETA; CELL-LINE; DAMAGE TOLERANCE; DEAMINASE AID; POL-ETA; UBIQUITIN; MICE; ACTIVATION; REPAIR
Sprache englisch
Veröffentlichungsjahr 2006
HGF-Berichtsjahr 2006
ISSN (print) / ISBN 0027-8424
e-ISSN 1091-6490
Zeitschrift Proceedings of the National Academy of Sciences of the United States of America
Quellenangaben Band: 103, Heft: 32, Seiten: 12081-12086 Artikelnummer: , Supplement: ,
Verlag National Academy of Sciences
Begutachtungsstatus Peer reviewed
Institut(e) Institute of Clinical Molecular Biology and Tumor Genetics (K.MOLBI)
POF Topic(s) 30504 - Mechanisms of Genetic and Environmental Influences on Health and Disease
Forschungsfeld(er) Immune Response and Infection
PSP-Element(e) G-501400-001
PubMed ID 16873544
DOI 10.1073/pnas.0605146103
WOS ID 000239701900047
Scopus ID 33747063573
Erfassungsdatum 2006-09-19
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