ArticleJournal of bacteriology2010
Sigma factor F does not prevent rifampin inhibition of RNA polymerase or cause rifampin tolerance in Mycobacterium tuberculosis.
Article in Journal of bacteriology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Bimodality in E. coli gene expression: Sources and robustness to genome-wide stresses.PLoS computational biology · 2025Article
- Transcription Attenuation in Synthetic Promoters in Nonoverlapping Tandem Formation.Biochemistry · 2024Article
- Transcriptional regulation and drug resistance inFrontiers in cellular and infection microbiology · 2022Review
- Mechanisms of Drug-Induced Tolerance in Mycobacterium tuberculosis.Clinical microbiology reviews · 2020Review
- Defining the Transcriptional and Post-transcriptional Landscapes ofFrontiers in microbiology · 2019Article
- Article
- Role of intragenic binding of cAMP responsive protein (CRP) in regulation of the succinate dehydrogenase genes Rv0249c-Rv0247c in TB complex mycobacteria.Nucleic acids research · 2015Article
- Genome-wide definition of the SigF regulon in Mycobacterium tuberculosis.Journal of bacteriology · 2012Article
- Virulence regulator EspR of Mycobacterium tuberculosis is a nucleoid-associated protein.PLoS pathogens · 2012Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The tolerance of Mycobacterium tuberculosis to antituberculosis drugs is a major reason for the lengthy therapy needed to treat a tuberculosis infection. Rifampin is a potent inhibitor of RNA polymerase (RNAP) in vivo but has been shown to be less effective against stationary-phase bacteria. Sigma factor F is associated with bacteria entering stationary phase and has been proposed to impact rifampin activity. Here we investigate whether RNAP containing SigF is more resistant to rifampin inhibition in vitro and whether overexpression of sigF renders M. tuberculosis more tolerant to rifampin. Real-time and radiometric in vitro transcription assays revealed that rifampin equally inhibits transcription by RNAP containing sigma factors SigA and SigF, therefore ruling out the hypothesis that SigF may be responsible for increased resistance of the enzyme to rifampin in vitro. In addition, overexpression or deletion of sigF did not alter rifampin susceptibility in axenic cultures of M. tuberculosis, indicating that SigF does not affect rifampin tolerance in vivo.
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