ArticleTuberculosis (Edinburgh, Scotland)2011
Mycobacterium tuberculosis gene Rv2136c is dispensable for acid resistance and virulence in mice.
Article in Tuberculosis (Edinburgh, Scotland), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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5 citing papers in PubMed.
- Cell wall peptidoglycan in Mycobacterium tuberculosis: An Achilles' heel for the TB-causing pathogen.FEMS microbiology reviews · 2019Review
- Characterization of blue light irradiation effects on pathogenic and nonpathogenic Escherichia coli.MicrobiologyOpen · 2017Article
- Functional characterization of two members of histidine phosphatase superfamily in Mycobacterium tuberculosis.BMC microbiology · 2013Article
- Article
- Computational comparative study of tuberculosis proteomes using a model learned from signal peptide structures.PloS one · 2012Article
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4 authors.
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Abstract
The gene Rv2136c is annotated to encode the Mycobacterium tuberculosis (Mtb) homolog of Escherichia coli's undecaprenyl pyrophosphate phosphatase. In previous work, a genetic screen of 10,100 Mtb transposon mutants identified Rv2136c as being involved in acid resistance in Mtb. The Rv2136c:Tn strain was also sensitive to sodium dodecyl sulfate, lipophilic antibiotics, elevated temperature and reactive oxygen and nitrogen intermediates and was attenuated for growth and persistence in mice. However, none of these phenotypes could be genetically complemented, leading us to generate an Rv2136c knockout strain to test its role in Mtb pathogenicity. Genetic deletion revealed that Rv2136c is not responsible for any of the phenotypes observed in the transposon mutant strain. An independent genomic mutation is likely to have accounted for the extreme attenuation of this strain. Identification of the mutated gene will further our understanding of acid resistance mechanisms in Mtb and may offer a target for anti-tuberculosis chemotherapy.
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