ArticlePloS one2017
The transcriptional regulator LysG (Rv1985c) of Mycobacterium tuberculosis activates lysE (Rv1986) in a lysine-dependent manner.
Article in PloS one, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed.
- Enhanced production of l-histidine inSynthetic and systems biotechnology · 2026Article
- LysG-driven transcriptional network rewiring underlies lineage-specific phenotypes in Mycobacterium tuberculosis.Nature communications · 2026Article
- The Diagnostic Value of Interleukin-2 and Interferon-γ Induced by Fusion Protein (ESAT-6/CFP-10/Rv1985c) for Active Mycobacterium tuberculosis Infection.Journal of clinical laboratory analysis · 2025Article
- Review
- Article
- CRISPR Interference-Based Inhibition of MAB_0055c Expression Alters Drug Sensitivity in Mycobacterium abscessus.Microbiology spectrum · 2023Article
- Derailing the aspartate pathway of Mycobacterium tuberculosis to eradicate persistent infection.Nature communications · 2019Article
- Physiology and Transcriptional Analysis of (p)ppGpp-Related Regulatory Effects inFrontiers in microbiology · 2019Article
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Authors and funding
5 authors.
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Abstract
The Mycobacterium tuberculosis protein encoded by the Rv1986 gene is a target for memory T cells in patients with tuberculosis, and shows strong similarities to a lysine exporter LysE of Corynebacterium glutamicum. During infection, the pathogen Mycobacterium tuberculosis adapts its metabolism to environmental changes. In this study, we found that the expression of Rv1986 is controlled by Rv1985c. Rv1985c is located directly upstream of Rv1986 with an overlapping promoter region between both genes. Semiquantitative reverse transcription PCR using an isogenic mutant of Mycobacterium tuberculosis lacking Rv1985c showed that in the presence of lysine, Rv1985c protein positively upregulated the expression of Rv1986. RNA sequencing revealed the transcription start points for both transcripts and overlapping promoters. An inverted repeat in the center of the intergenic region was identified, and binding of Rv1985c protein to the intergenic region was confirmed by electrophoretic mobility shift assays. Whole transcriptome expression analysis and RNAsequencing showed downregulated transcription of ppsBCD in the Rv1985c-mutant compared to the wild type strain. Taken together, our findings characterize the regulatory network of Rv1985c in Mycobacterium tuberculosis. Due to their similarity of an orthologous gene pair in Corynebacterium glutamicum, we suggest to rename Rv1985c to lysG(Mt), and Rv1986 to lysE(Mt).
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