A RECA PROTEIN MUTANT DEFICIENT IN ITS INTERACTION WITH THE UMUDC COMPLEX

被引：70

作者：

BAILONE, A ^{[1
]}

SOMMER, S ^{[1
]}

KNEZEVIC, J ^{[1
]}

DUTREIX, M ^{[1
]}

DEVORET, R ^{[1
]}

机构：

[1] CNRS,ENZYMOL LAB,ETUD MUTAGENES & CANCEROGENES GRP,F-91198 GIF SUR YVETTE,FRANCE

来源：

BIOCHIMIE | 1991年 / 73卷 / 04期

关键词：

MUT- DOMINANT PHENOTYPE; RECA FUNCTIONS; COMPLEMENTATION OF RECA MUTATIONS; UMUD' FORMATION; PKM101; PLASMID;

D O I：

10.1016/0300-9084(91)90115-H

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

recA1730 is a dominant point mutation preventing SOS mutagenesis. We demonstrate here that: i) RecA1730 fails to produce mutagenesis even though UmuD' is formed, ii) recA1730, when complemented by recA+, can cleave LexA protein and it displays a UmuDC-phenotype in spite of adequate concentrations of matured UmuD' and UmuC proteins, iii) the Mut- phenotype caused by RecA1730 is partially alleviated by MucAB proteins, functional analogs of UmuDC. To explain the mutant phenotype, we postulate that recA1730 impairs a RecA function required for the positioning of the UmuD'C complex within the replisome at the site of lesions.

引用

页码：479 / 484

页数：6

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