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


Davis, E O; Springer, B; Gopaul, K K; Papavinasasundaram, K G; Sander, P; Böttger, E C (2002). DNA damage induction of recA in Mycobacterium tuberculosis independently of RecA and LexA. Molecular Microbiology, 46(3):791-800.

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.

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.

Citations

38 citations in Web of Science®
40 citations in Scopus®
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Additional indexing

Item Type:Journal Article, refereed, original work
Communities & Collections:04 Faculty of Medicine > Institute of Medical Microbiology
Dewey Decimal Classification:570 Life sciences; biology
610 Medicine & health
Language:English
Date:2002
Deposited On:26 Mar 2009 13:13
Last Modified:05 Apr 2016 12:29
Publisher:Wiley-Blackwell
ISSN:0950-382X
Publisher DOI:https://doi.org/10.1046/j.1365-2958.2002.03199.x
PubMed ID:12410836

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