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结核分枝杆菌中recA的DNA损伤诱导独立于RecA和LexA。

DNA damage induction of recA in Mycobacterium tuberculosis independently of RecA and LexA.

作者信息

Davis Elaine O, Springer Burkhard, Gopaul Krishna K, Papavinasasundaram K G, Sander Peter, Böttger Erik C

机构信息

Division of Mycobacterial Research, National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, UK.

出版信息

Mol Microbiol. 2002 Nov;46(3):791-800. doi: 10.1046/j.1365-2958.2002.03199.x.

DOI:10.1046/j.1365-2958.2002.03199.x
PMID:12410836
Abstract

The ubiquitous and highly conserved RecA protein is generally expressed from a single promoter, which is regulated by LexA in conjunction with RecA. We show here using transcriptional fusions to a reporter gene that the Mycobacterium tuberculosis recA gene is expressed from two promoters. Although one promoter is clearly regulated in the classical way, the other remains DNA damage inducible in the absence of RecA or when LexA binding is prevented. These observations demonstrate convincingly for the first time that there is a novel mechanism of DNA damage induction in M. tuberculosis that is independent of LexA and RecA.

摘要

普遍存在且高度保守的RecA蛋白通常由单个启动子表达,该启动子由LexA与RecA共同调控。我们在此利用与报告基因的转录融合表明,结核分枝杆菌recA基因由两个启动子表达。虽然一个启动子显然以经典方式受到调控,但另一个在没有RecA或LexA结合被阻止时仍可被DNA损伤诱导。这些观察结果首次令人信服地证明,结核分枝杆菌中存在一种独立于LexA和RecA的新型DNA损伤诱导机制。

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