Identification of a promoter motif regulating the major DNA damage response mechanism of Mycobacterium tuberculosis

• Published in: FEMS microbiology letters Vol. 238; no. 1; pp. 57 - 63
• Main Authors: Gamulin, Vera, Cetkovic, Helena, Ahel, Ivan
• Format: Journal Article
• Language: English
• Published: Oxford, UK Blackwell Publishing Ltd 01.09.2004; Blackwell; Oxford University Press
• Subjects: Actinomycetales; Actinomycetales - genetics; Bacterial Proteins - genetics; Bacterial Proteins - metabolism; Bacterial Proteins - physiology; Bacteriology; Base Sequence; Biological and medical sciences; Consensus Sequence; Deoxyribonucleic acid; DNA; DNA Damage; DNA damage response; DNA repair; DNA Repair - genetics; Fundamental and applied biological sciences. Psychology; Gene Expression Regulation, Bacterial; Genes; Genetics; Humans; Microbiology; Molecular Sequence Data; Mycobacterium tuberculosis; Mycobacterium tuberculosis - genetics; Mycobacterium tuberculosis - metabolism; Promoter; Promoter Regions, Genetic; Rec A Recombinases - genetics; Rec A Recombinases - metabolism; RecA; RecA protein; Regulon; Repair; Sequence Alignment; Serine Endopeptidases - genetics; Serine Endopeptidases - metabolism; Sigma Factor - physiology; Tuberculosis; Promoter; Actinomycetales; Tuberculosis; DNA damage response; RecA; Transcription promoter; Mycobacterial infection; Genetic determinism; Infection; Sequential analysis; Structural unit; Mycobacterium tuberculosis; Mycobacteriales; RecA protein; Bacteriosis; Mycobacteriaceae; Bacteria; SOS function; Actinomycetes
• ISSN: 0378-1097; 1574-6968
• DOI: 10.1111/j.1574-6968.2004.tb09737.x

Abstract The principal response of many bacteria to DNA damage is mediated by a mechanism dependent on the LexA and RecA proteins. However, Mycobacterium tuberculosis was recently reported to regulate a majority of DNA repair genes independently of RecA and LexA, suggesting that an unknown RecA/LexA-independent mechanism controls the major DNA damage response pathway in this organism. Here we have identified a motif tTGTCRgtg-8nt-TAnnnT that defines a novel RecA/LexA-independent promoter (RecA-NDp) of M. tuberculosis. Furthermore, we show that the RecA-NDp type of promoter precedes DNA repair genes in other Actinomycetales.