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在大肠杆菌K-12中,recA4162(I298V)和recA4164(L126V)对组成型SOS表达的抑制需要UvrD和RecX。

Suppression of constitutive SOS expression by recA4162 (I298V) and recA4164 (L126V) requires UvrD and RecX in Escherichia coli K-12.

作者信息

Long Jarukit E, Renzette Nicholas, Sandler Steven J

机构信息

Department of Microbiology, Morrill Science Center IV N203, University of Massachusetts at Amherst, Amherst, MA 01003, USA.

出版信息

Mol Microbiol. 2009 Jul;73(2):226-39. doi: 10.1111/j.1365-2958.2009.06765.x. Epub 2009 Jun 23.

Abstract

Sensing DNA damage and initiation of genetic responses to repair DNA damage are critical to cell survival. In Escherichia coli, RecA polymerizes on ssDNA produced by DNA damage creating a RecA-DNA filament that interacts with the LexA repressor inducing the SOS response. RecA filament stability is negatively modulated by RecX and UvrD. recA730 (E38K) and recA4142 (F217Y) constitutively express the SOS response. recA4162 (I298V) and recA4164 (L126V) are intragenic suppressors of the constitutive SOS phenotype of recA730. Herein, it is shown that these suppressors are not allele specific and can suppress SOS(C) expression of recA730 and recA4142 in cis and in trans. recA4162 and recA4164 single mutants (and the recA730 and recA4142 derivatives) are Rec(+), UV(R) and are able to induce the SOS response after UV treatment like wild-type. UvrD and RecX are required for the suppression in two (recA730,4164 and recA4142,4162) of the four double mutants tested. To explain the data, one model suggests that recA(C) alleles promote SOS(C) expression by mimicking RecA filament structures that induce SOS and the suppressor alleles mimic RecA filament at end of SOS. UvrD and RecX are attracted to these latter structures to help dismantle or destabilize the RecA filament.

摘要

感知DNA损伤并启动对DNA损伤进行修复的遗传反应对于细胞存活至关重要。在大肠杆菌中,RecA在DNA损伤产生的单链DNA上聚合,形成RecA-DNA细丝,该细丝与LexA阻遏物相互作用,诱导SOS反应。RecA细丝的稳定性受到RecX和UvrD的负调控。recA730(E38K)和recA4142(F217Y)组成型表达SOS反应。recA4162(I298V)和recA4164(L126V)是recA730组成型SOS表型的基因内抑制子。本文表明,这些抑制子不是等位基因特异性的,能够在顺式和反式中抑制recA730和recA4142的SOS(C)表达。recA4162和recA4164单突变体(以及recA730和recA4142衍生物)是Rec(+)、UV(R),并且能够像野生型一样在紫外线处理后诱导SOS反应。在所测试的四个双突变体中的两个(recA730,4164和recA4142,4162)中,抑制作用需要UvrD和RecX。为了解释这些数据,一个模型表明,recA(C)等位基因通过模拟诱导SOS的RecA细丝结构来促进SOS(C)表达,而抑制子等位基因在SOS结束时模拟RecA细丝。UvrD和RecX被吸引到这些后者的结构上,以帮助拆解或破坏RecA细丝的稳定性。

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