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Titolo:
Repair of chromosomal abasic sites in vivo involves at least three different repair pathways
Autore:
Otterlei, M; Kavli, B; Standal, R; Skjelbred, C; Bharati, S; Krokan, HE;
Indirizzi:
Norwegian Univ Sci & Technol, Fac Med, Inst Canc Res & Mol Biol, N-7489 Trondheim, Norway Norwegian Univ Sci & Technol Trondheim Norway N-7489 9 Trondheim, Norway
Titolo Testata:
EMBO JOURNAL
fascicolo: 20, volume: 19, anno: 2000,
pagine: 5542 - 5551
SICI:
0261-4189(20001016)19:20<5542:ROCASI>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
URACIL-DNA GLYCOSYLASE; APURINIC APYRIMIDINIC SITES; COLI RNA-POLYMERASE; ESCHERICHIA-COLI; EXONUCLEASE-III; BETA-SUBUNIT; BASE-DAMAGE; DINB GENE; MUTAGENESIS; MUTANTS;
Keywords:
AP-endonuclease; chromosomal abasic site; recombination; translesion DNA synthesis; UmuC;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Krokan, HE Norwegian Univ Sci & Technol, Fac Med, Inst Canc Res & Mol Biol, N-7489 Trondheim, Norway Norwegian Univ Sci & Technol Trondheim Norway N-7489 , Norway
Citazione:
M. Otterlei et al., "Repair of chromosomal abasic sites in vivo involves at least three different repair pathways", EMBO J, 19(20), 2000, pp. 5542-5551

Abstract

We introduced multiple abasic sites (AP sites) in the chromosome of repair-deficient mutants of Escherichia coli, in vivo, by expressing engineered variants of uracil-DNA glycosylase that remove either thymine or cytosine. After introduction of AP sites, deficiencies in base excision repair (BER) or recombination were associated with strongly enhanced cytotoxicity and elevated mutation frequencies, selected as base substitutions giving rifampicin resistance. In these strains, increased fractions of transversions and untargeted mutations were observed. In a recA mutant, deficient in both recombination and translesion DNA synthesis (TLS), multiple AP sites resulted inrapid cell death. Preferential incorporation of dAMP opposite a chromosomal AP site ('A rule') required UmuC. Furthermore, we observed an 'A rule-like' pattern of spontaneous mutations that was also UmuC dependent. The mutation patterns indicate that UmuC is involved in untargeted mutations as well. In a UmuC-deficient background, a preference for dGMP was observed. Spontaneous mutation spectra were generally strongly dependent upon the repair background. In conclusion, BER, recombination and TLS all contribute to the handling of chromosomal AP sites in E.coli in vivo.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/12/20 alle ore 01:04:13