Identification of some DNA damage-inducible genes of Mycobacterium tuberculosis: Apparent lack of correlation with LexA binding

Citation
Pc. Brooks et al., Identification of some DNA damage-inducible genes of Mycobacterium tuberculosis: Apparent lack of correlation with LexA binding, J BACT, 183(15), 2001, pp. 4459-4467
Citations number
34
Categorie Soggetti
Microbiology
Journal title
JOURNAL OF BACTERIOLOGY
ISSN journal
00219193 → ACNP
Volume
183
Issue
15
Year of publication
2001
Pages
4459 - 4467
Database
ISI
SICI code
0021-9193(200108)183:15<4459:IOSDDG>2.0.ZU;2-7
Abstract
The repair of DNA damage is expected to be particularly important to intrac ellular pathogens such as Mycobacterium tuberculosis, and so it is of inter est to examine the response of M. tuberculosis to DNA damage. The expressio n of recA, a key component in DNA repair and recombination, is induced by D NA damage in M. tuberculosis. In this study, we have analyzed the expressio n following DNA damage in M. tuberculosis of a number of other genes which are DNA damage inducible in Escherichia coli, While many of these genes wer e also induced by DNA damage in M, tuberculosis, some were not. In addition , one gene (ruvC) which is not induced by DNA damage in E. coli was induced in M, tuberculosis, a result likely linked to its different transcriptiona l arrangement in M. tuberculosis. We also searched the sequences upstream o f the genes being studied for the mycobacterial SOS box (the binding site f or LexA) and assessed LexA binding to potential sites identified. LexA is t he repressor protein responsible for regulating expression of these SOS gen es in E. coli. However, two of the genes which were DNA damage inducible in M. tuberculosis did not have identifiable sites to which LexA bound. The a bsence of binding sites for LexA upstream of these genes aas confirmed by a nalysis of LexA binding to overlapping DNA fragments covering a region from 500 bp upstream of the coding sequence to 100 bp within it. Therefore, it appears most likely that an alternative mechanism of gene regulation in res ponse to DNA damage exists in M. tuberculosis.