ArticleThe Journal of biological chemistry2016
The Structure of the Transcriptional Repressor KstR in Complex with CoA Thioester Cholesterol Metabolites Sheds Light on the Regulation of Cholesterol Catabolism in Mycobacterium tuberculosis.
Article in The Journal of biological chemistry, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 36 citations in OpenAlex.
- Degradation of CCurrent microbiology · 2025Article
- Exploiting cAMP signaling in Mycobacterium tuberculosis for drug discovery.Trends in microbiology · 2024Review
- Rerouting phytosterol degradation pathway for directed androst-1,4-diene-3,17-dione microbial bioconversion.Applied microbiology and biotechnology · 2024Article
- The impact ofFrontiers in immunology · 2024Review
- Mce1R of Mycobacterium tuberculosis prefers long-chain fatty acids as specific ligands: a computational study.Molecular diversity · 2023Article
- Article
- Insight into Different Stages of Steroid Degradation in ThermophilicInternational journal of molecular sciences · 2022Article
- Iron limitation in M. tuberculosis has broad impact on central carbon metabolism.Communications biology · 2022Article
- Further Studies on the 3-Ketosteroid 9α-Hydroxylase ofMicroorganisms · 2021Article
- The Operon Encoding Hydrolytic Dehalogenation of 4-Chlorobenzoate Is Transcriptionally Regulated by the TetR-Type Repressor FcbR and Its Ligand 4-Chlorobenzoyl Coenzyme A.Applied and environmental microbiology · 2021Article
- A Förster Resonance Energy Transfer-Based Ratiometric Sensor with the Allosteric Transcription Factor TetR.Small (Weinheim an der Bergstrasse, Germany) · 2020Article
- Engineering DNA recognition and allosteric response properties of TetR family proteins by using a module-swapping strategy.Nucleic acids research · 2019Article
- Review
- Cholesterol and fatty acids grease the wheels of Mycobacterium tuberculosis pathogenesis.Pathogens and disease · 2018Review
- Cholesterol metabolism: a potential therapeutic target in Mycobacteria.British journal of pharmacology · 2017Review
- Article
- Functional differentiation of 3-ketosteroid ΔMicrobial cell factories · 2017Article
- The AibR-isovaleryl coenzyme A regulator and its DNA binding site - a model for the regulation of alternative de novo isovaleryl coenzyme A biosynthesis in Myxococcus xanthus.Nucleic acids research · 2017Article
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Authors and funding
9 authors at 4 institutions in 3 countries.
Funding
Abstract
Cholesterol can be a major carbon source forMycobacterium tuberculosisduring infection, both at an early stage in the macrophage phagosome and later within the necrotic granuloma. KstR is a highly conserved TetR family transcriptional repressor that regulates a large set of genes responsible for cholesterol catabolism. Many genes in this regulon, includingkstR, are either induced during infection or are essential for survival ofM. tuberculosis in vivo In this study, we identified two ligands for KstR, both of which are CoA thioester cholesterol metabolites with four intact steroid rings. A metabolite in which one of the rings was cleaved was not a ligand. We confirmed the ligand-protein interactions using intrinsic tryptophan fluorescence and showed that ligand binding strongly inhibited KstR-DNA binding using surface plasmon resonance (IC50for ligand = 25 nm). Crystal structures of the ligand-free form of KstR show variability in the position of the DNA-binding domain. In contrast, structures of KstR·ligand complexes are highly similar to each other and demonstrate a position of the DNA-binding domain that is unfavorable for DNA binding. Comparison of ligand-bound and ligand-free structures identifies residues involved in ligand specificity and reveals a distinctive mechanism by which the ligand-induced conformational change mediates DNA release.
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