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Titolo:
Rad52 partially substitutes for the Rad51 paralog XRCC3 in maintaining chromosomal integrity in vertebrate cells
Autore:
Fujimori, A; Tachiiri, S; Sonoda, E; Thompson, LH; Dhar, PK; Hiraoka, M; Takeda, S; Zhang, Y; Reth, M; Takata, M;
Indirizzi:
Kyoto Univ, Fac Med, Dept Radiat Genet, Sakyo Ku, Kyoto 6068501, Japan Kyoto Univ Kyoto Japan 6068501 iat Genet, Sakyo Ku, Kyoto 6068501, Japan Kyoto Univ, Fac Med, Dept Therapeut Radiol & Oncol, Sakyo Ku, Kyoto 6068507, Japan Kyoto Univ Kyoto Japan 6068507 l & Oncol, Sakyo Ku, Kyoto 6068507, Japan JST, CREST, Saitama, Japan JST Saitama JapanJST, CREST, Saitama, Japan Lawrence Livermore Natl Lab, BBR Program, Livermore, CA 94551 USA LawrenceLivermore Natl Lab Livermore CA USA 94551 ivermore, CA 94551 USA Univ Freiburg, Dept Mol Immunol, D-79108 Freiburg, Germany Univ Freiburg Freiburg Germany D-79108 mmunol, D-79108 Freiburg, Germany Max Planck Inst Immunbiol, D-79108 Freiburg, Germany Max Planck Inst Immunbiol Freiburg Germany D-79108 108 Freiburg, Germany
Titolo Testata:
EMBO JOURNAL
fascicolo: 19, volume: 20, anno: 2001,
pagine: 5513 - 5520
SICI:
0261-4189(20011001)20:19<5513:RPSFTR>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
REPLICATION PROTEIN-A; DOUBLE-STRAND BREAKS; DNA-REPAIR GENE; HOMOLOGOUS RECOMBINATION; SACCHAROMYCES-CEREVISIAE; MOUSE GENES; FAMILY; PATHWAY; MEMBER; RECA;
Keywords:
DT40; homologous recombination; Rad51 paralogs; Rad52; XRCC3;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
56
Recensione:
Indirizzi per estratti:
Indirizzo: Takata, M Kawasaki Med Univ, Dept Immunol & Mol Genet, 577 Matsushima, Kurashiki, Okayama 7010192, Japan Kawasaki Med Univ 577 Matsushima Kurashiki Okayama Japan 7010192
Citazione:
A. Fujimori et al., "Rad52 partially substitutes for the Rad51 paralog XRCC3 in maintaining chromosomal integrity in vertebrate cells", EMBO J, 20(19), 2001, pp. 5513-5520

Abstract

Yeast Rad52 DNA-repair mutants exhibit pronounced radiation sensitivity and a defect in homologous recombination (HR), whereas vertebrate cells lacking Rad52 exhibit a nearly normal phenotype. Biochemical studies show that both yeast Rad52 and Rad55-57 (Rad51 paralogs) stimulate DNA-strand exchangemediated by Rad51. These findings raise the possibility that Rad51 paralogs may compensate for lack of Rad52 in vertebrate cells, explaining the absence of prominent phenotypes for Rad52-deficient cells. To test this hypothesis, using chicken DT40 cells, we generated conditional mutants deficient in both RAD52 and XRCC3, which is one of the five vertebrate PAD51 paralogs. Surprisingly, the rad52 xrcc3 double-mutant cells were non-viable and exhibited extensive chromosomal breaks, whereas rad52 and xrcc3 single mutants grew well. Our data reveal an overlapping (but non-reciprocal) role for Rad52 and XRCC3 in repairing DNA double-strand breaks. The present study showsthat Rad52 can play an important role in HR repair by partially substituting for a Rad51 paralog.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 25/11/20 alle ore 18:36:15