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Titolo:
Alteration of ultraviolet-induced mutagenesis in yeast through molecular modulation of the REV3 and REV7 gene expression
Autore:
Rajpal, DK; Wu, XH; Wang, ZG;
Indirizzi:
Univ Kentucky, Grad Ctr Toxicol, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 Ctr Toxicol, Lexington, KY 40536 USA
Titolo Testata:
MUTATION RESEARCH-DNA REPAIR
fascicolo: 2, volume: 461, anno: 2000,
pagine: 133 - 143
SICI:
0921-8777(20001016)461:2<133:AOUMIY>2.0.ZU;2-A
Fonte:
ISI
Lingua:
ENG
Soggetto:
DAMAGE-INDUCED MUTAGENESIS; THYMINE-THYMINE DIMER; DNA-POLYMERASE-ZETA; 2 HUMAN HOMOLOGS; SACCHAROMYCES-CEREVISIAE; XERODERMA-PIGMENTOSUM; MOUSE HOMOLOGS; PROTEIN; ENCODES; BINDING;
Keywords:
mutagenesis; UV damage; DNA polymerase zeta; deoxycytidyl transferase;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
35
Recensione:
Indirizzi per estratti:
Indirizzo: Wang, ZG Univ Kentucky, Grad Ctr Toxicol, Lexington, KY 40536 USA Univ Kentucky Lexington KY USA 40536 ol, Lexington, KY 40536 USA
Citazione:
D.K. Rajpal et al., "Alteration of ultraviolet-induced mutagenesis in yeast through molecular modulation of the REV3 and REV7 gene expression", MUT R-DNA R, 461(2), 2000, pp. 133-143

Abstract

DNA damage can lead to mutations during replication. The damage-induced mutagenesis pathway is an important mechanism that fixes DNA lesions into mutations. DNA polymerase zeta (Pol zeta), formed by Rev3 and Rev7 protein complex, and Rev1 are components of the damage-induced mutagenesis pathway. Since mutagenesis is an important factor during the initiation and progression of human cancer, we postulate that this mutagenesis pathway may provide an inhibiting target for cancer prevention and therapy. In this study, we tested if UV-induced mutagenesis can be altered by molecular modulation of Rev3 enzyme levels using the yeast Saccharomyces cerevisiae as a eukaryotic model system. Reducing the REV3 expression in yeast cells through molecular techniques was employed to mimic Pol zeta inhibition. Lower levels of Pol zeta significantly decreased UV-induced mutation frequency, thus achieving inhibition of mutagenesis. In contrast, elevating the Pol zeta level by enhanced expression of both REV3 and REV7 genes led to a similar to 3-fold increase in UV-induced mutagenesis as determined by the arg4-17 mutation reversion assays. In vivo, UV lesion bypass by Pol zeta requires the Rev1 protein. Even overexpression of Pol zeta could not alleviate the defective UV mutagenesis in the rev1 mutant cells. These observations provide evidence that the mutagenesis pathway could be used as a target for inhibiting damage-induced mutations. (C) 2000 Elsevier Science B.V. All rights reserved.

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Documento generato il 05/04/20 alle ore 00:39:08