Role of stress response sigma factor SigG in Mycobacterium tuberculosis.

Jong-Hee Lee, Deborah E Geiman, William R Bishai
Author Information
  1. Jong-Hee Lee: Department of Medicine, Division of Infectious Diseases, Johns Hopkins School of Medicine, CRB2, Room 1.08, 1550 Orleans Street, Baltimore, MD 21231-1044, USA.

Abstract

The sigG gene of Mycobacterium tuberculosis was disrupted by homologous recombination, and the genes regulated by SigG were examined by real-time reverse-transcription PCR and microarray studies. The SigG consensus promoter recognition sequence was identified as GCGNGT-N15-18-CGANCA. A DeltasigG mutant was found to be more resistant to mitomycin C treatment than the wild-type strain, indicating that it may be involved in the SOS response in M. tuberculosis.

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Grants

  1. R01 AI043846/NIAID NIH HHS
  2. AI37856/NIAID NIH HHS
  3. R01 AI037856/NIAID NIH HHS
  4. R01 AI036973/NIAID NIH HHS
  5. AI43846/NIAID NIH HHS
  6. AI36973/NIAID NIH HHS

MeSH Term

Animals
Bacterial Proteins
Base Sequence
Cell Line
DNA-Directed RNA Polymerases
Gene Expression Regulation, Bacterial
Heat-Shock Response
Humans
Macrophages, Alveolar
Mice
Molecular Sequence Data
Mycobacterium tuberculosis
Oligonucleotide Array Sequence Analysis
Promoter Regions, Genetic
Recombination, Genetic
Reverse Transcriptase Polymerase Chain Reaction
SOS Response, Genetics
Sigma Factor

Chemicals

Bacterial Proteins
Sigma Factor
RNA polymerase sigma 70
DNA-Directed RNA Polymerases

Word Cloud

Created with Highcharts 10.0.0tuberculosisSigGMycobacteriumresponsesigGgenedisruptedhomologousrecombinationgenesregulatedexaminedreal-timereverse-transcriptionPCRmicroarraystudiesconsensuspromoterrecognitionsequenceidentifiedGCGNGT-N15-18-CGANCADeltasigGmutantfoundresistantmitomycinCtreatmentwild-typestrainindicatingmayinvolvedSOSMRolestresssigmafactor

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