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DNA damage induction of recA in Mycobacterium tuberculosis independently of RecA and LexA
Author(s) -
Davis Elaine O.,
Springer Burkhard,
Gopaul Krishna K.,
Papavinasasundaram K. G.,
Sander Peter,
Böttger Erik C.
Publication year - 2002
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1046/j.1365-2958.2002.03199.x
Subject(s) - repressor lexa , biology , sos response , promoter , mycobacterium tuberculosis , gene , dna , genetics , repressor , dna damage , microbiology and biotechnology , gene expression , tuberculosis , medicine , pathology
Summary 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.