ArticleInfection and immunity2014
A specific polymorphism in Mycobacterium tuberculosis H37Rv causes differential ESAT-6 expression and identifies WhiB6 as a novel ESX-1 component.
Article in Infection and immunity, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers.
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Who cites it
50 citing papers in PubMed, 100 citations in OpenAlex.
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- The regulatory functions of ESX-1 substrates, EspE and EspF, are separable from secretion.Journal of bacteriology · 2024Article
- The antagonistic transcription factors, EspM and EspN, regulate the ESX-1 secretion system inmBio · 2024Article
- ESAT-6 a Major Virulence Factor ofBiomolecules · 2023Review
- Immunopeptidomics reveals determinants ofeLife · 2023Article
- Functional Analysis of EspM, an ESX-1-Associated Transcription Factor in Mycobacterium marinum.Journal of bacteriology · 2022Article
- Bacterial secretion systems: Networks of pathogenic regulation and adaptation in mycobacteria and beyond.PLoS pathogens · 2022Article
- TheMolecular therapy. Nucleic acids · 2022Article
- The Lack of the TetR-Like Repressor GeneFrontiers in cellular and infection microbiology · 2022Article
- Type VII secretion systems: structure, functions and transport models.Nature reviews. Microbiology · 2021Review
- Engineering a new vaccine platform for heterologous antigen delivery in live-attenuatedComputational and structural biotechnology journal · 2021Article
- Modeling Tubercular ESX-1 Secretion Using Mycobacterium marinum.Microbiology and molecular biology reviews : MMBR · 2020Review
Corrections and comments
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Authors and funding
8 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The ESX-1 secreted virulence factor ESAT-6 is one of the major and most well-studied virulence factors of Mycobacterium tuberculosis, given that its inactivation severely attenuates virulent mycobacteria. In this work, we show that clinical isolates of M. tuberculosis produce and secrete larger amounts of ESAT-6 than the widely used M. tuberculosis H37Rv laboratory strain. A search for the genetic polymorphisms underlying this observation showed that whiB6 (rv3862c), a gene upstream of the ESX-1 genetic locus that has not previously been found to be implicated in the regulation of the ESX-1 secretory apparatus, presents a unique single nucleotide insertion in its promoter region in strains H37Rv and H37Ra. This polymorphism is not present in any of the other publicly available M. tuberculosis complex genomes or in any of the 76 clinical M. tuberculosis isolates analyzed in our laboratory. We demonstrate that in consequence, the virulence master regulator PhoP downregulates whiB6 expression in H37Rv, while it upregulates its expression in clinical strains. Importantly, reintroduction of the wild-type (WT) copy of whiB6 in H37Rv restored ESAT-6 production and secretion to the level of clinical strains. Hence, we provide clear evidence that in M. tuberculosis--with the exception of the H37Rv strain--ESX-1 expression is regulated by WhiB6 as part of the PhoP regulon, which adds another level of complexity to the regulation of ESAT-6 secretion with a potential role in virulence adaptation.
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