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Journal of Bacteriology, June 2002, p. 3287-3295, Vol. 184, No. 12
0021-9193/02/$04.00+0 DOI: 10.1128/JB.184.12.3287-3295.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
Definition of the Mycobacterial SOS Box and Use To Identify LexA-Regulated Genes in Mycobacterium tuberculosis
Elaine O. Davis,* Edith M. Dullaghan,,
and Lucinda Rand
Division of Mycobacterial Research, National Institute for Medical Research, London NW7 1AA, England
Received 4 January 2002/
Accepted 29 March 2002
The bases of the mycobacterial SOS box important for LexA binding were determined by replacing each base with every other and examining the effect on the induction of a reporter gene following DNA damage. This analysis revealed that the SOS box was longer than originally thought by 2 bp in each half of the palindromic site. A search of the Mycobacterium tuberculosis genome sequence with the new consensus, TCGAAC(N)4GTTCGA, identified 4 sites which were perfect matches and 12 sites with a single mismatch which were predicted to bind LexA. Genes which could potentially be regulated by these SOS boxes were ascertained from their positions relative to the sites. Examination of expression data for these genes following DNA damage identified 12 new genes which are most likely regulated by LexA as well as the known M. tuberculosis DNA damage-inducible genes recA, lexA, and ruvC. Of these 12 genes, only 2 have a predicted function: dnaE2, a component of DNA polymerase III, and linB, which is similar to 1,3,4,6-tetrachloro-1,4-cylcohexadiene hydrolase. Curiously, of the remaining 10 genes predicted to be LexA regulated, 7 are members of the M. tuberculosis 13E12 repeat family, which has some of the characteristics of mobile elements.
* Corresponding author. Mailing address: Division of Mycobacterial Research, National Institute for Medical Research, The Ridgeway, Mill Hill, London NW7 1AA, England. Phone: 020 8959 3666. Fax: 020 8913 8528. E-mail:
edavis{at}nimr.mrc.ac.uk.
Present address: The Research Centre, Faculty of Medicine, Dept. of Paediatrics, The University of British Columbia, Vancouver, B.C., Canada V5Z 4H4.
Journal of Bacteriology, June 2002, p. 3287-3295, Vol. 184, No. 12
0021-9193/02/$04.00+0 DOI: 10.1128/JB.184.12.3287-3295.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.
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