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Literature DB >> 9084177

Characterization of Mycobacterium tuberculosis LexA: recognition of a Cheo (Bacillus-type SOS) box.

Farahnaz Movahedzadeh¹, M Joseph Colston¹, Elaine O Davis¹.

Abstract

The gene coding for the Mycobacterium tuberculosis homologue of LexA has been cloned and sequenced. Amino acids required for autocatalytic cleavage are conserved, whereas those important for specific DNA binding are not, when compared with Escherichia coli LexA. The transcriptional start site was mapped and a DNA sequence motif was identified which resembled the consensus Cheo box sequence involved in the regulation of DNA-damage-inducible genes in Bacillus subtilis. The M. tuberculosis-LexA protein was overexpressed in E. coli and purified by means of a His tag. The purified LexA was shown to bind to the Cheo box sequence found upstream of its own gene.

Entities: Disease Gene Species

Mesh：

Substances：

Year: 1997 PMID： 9084177 DOI： 10.1099/00221287-143-3-929

Source DB: PubMed Journal: Microbiology (Reading) ISSN： 1350-0872 Impact factor: 2.777

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Cited

19 in total

1. Crystallization and preliminary X-ray studies of the C-terminal domain of Mycobacterium tuberculosis LexA.

Authors: Anu V Chandran; J Rajan Prabu; G P Manjunath; K Neelakanteshwar Patil; K Muniyappa; M Vijayan
Journal: Acta Crystallogr Sect F Struct Biol Cryst Commun Date: 2010-08-28

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

Authors: P C Brooks; F Movahedzadeh; E O Davis
Journal: J Bacteriol Date: 2001-08 Impact factor: 3.490

3. Determination of DNA sequences required for regulated Mycobacterium tuberculosis RecA expression in response to DNA-damaging agents suggests that two modes of regulation exist.

Authors: F Movahedzadeh; M J Colston; E O Davis
Journal: J Bacteriol Date: 1997-06 Impact factor: 3.490

4. SigG does not control gene expression in response to DNA damage in Mycobacterium tuberculosis H37Rv.

Authors: Katherine L Smollett; Lisa F Dawson; Elaine O Davis
Journal: J Bacteriol Date: 2010-12-17 Impact factor: 3.490

5. Mycobacterial Mutagenesis and Drug Resistance Are Controlled by Phosphorylation- and Cardiolipin-Mediated Inhibition of the RecA Coprotease.

Authors: Matthew F Wipperman; Brook E Heaton; Astha Nautiyal; Oyindamola Adefisayo; Henry Evans; Richa Gupta; Dave van Ditmarsch; Rajesh Soni; Ron Hendrickson; Jeff Johnson; Nevan Krogan; Michael S Glickman
Journal: Mol Cell Date: 2018-08-30 Impact factor: 17.970

10. Experimental determination of translational start sites resolves uncertainties in genomic open reading frame predictions - application to Mycobacterium tuberculosis.

Authors: Katherine L Smollett; Amanda S Fivian-Hughes; Joanne E Smith; Anchi Chang; Tara Rao; Elaine O Davis
Journal: Microbiology (Reading) Date: 2009-01 Impact factor: 2.777

Characterization of Mycobacterium tuberculosis LexA: recognition of a Cheo (Bacillus-type SOS) box.

1. Crystallization and preliminary X-ray studies of the C-terminal domain of Mycobacterium tuberculosis LexA.

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

3. Determination of DNA sequences required for regulated Mycobacterium tuberculosis RecA expression in response to DNA-damaging agents suggests that two modes of regulation exist.

4. SigG does not control gene expression in response to DNA damage in Mycobacterium tuberculosis H37Rv.

5. Mycobacterial Mutagenesis and Drug Resistance Are Controlled by Phosphorylation- and Cardiolipin-Mediated Inhibition of the RecA Coprotease.

6. Definition of the mycobacterial SOS box and use to identify LexA-regulated genes in Mycobacterium tuberculosis.

7. Molecular characterization of the eis promoter of Mycobacterium tuberculosis.

8. Group I self-splicing intron in the recA gene of Bacillus anthracis.

9. The mycobacterium-specific gene Rv2719c is DNA damage inducible independently of RecA.

10. Experimental determination of translational start sites resolves uncertainties in genomic open reading frame predictions - application to Mycobacterium tuberculosis.