ArticleInfection and immunity2015
Mycobacterium tuberculosis Resists Stress by Regulating PE19 Expression.
Article in Infection and immunity, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 43 citations in OpenAlex.
- ThemBio · 2026Article
- Essential role of MHC II in the antitubercular efficacy of pyrazinamide.Antimicrobial agents and chemotherapy · 2026Article
- Prophylactic and post-exposure efficacy of a Pichinde virus vector-based tuberculosis vaccine.Frontiers in immunology · 2026Article
- Article
- The PE/PPE family proteins ofFrontiers in immunology · 2025Review
- Article
- Marine sponge microbe provides insights into evolution and virulence of the tubercle bacillus.PLoS pathogens · 2024Article
- Transposon sequencing reveals metabolic pathways essential for Mycobacterium tuberculosis infection.PLoS pathogens · 2024Article
- Recombinant Pichinde viral vector expressing tuberculosis antigens elicits strong T cell responses and protection in mice.Frontiers in immunology · 2023Article
- Delineating transcriptional crosstalk between Mycobacterium avium subsp. paratuberculosis and human THP-1 cells at the early stage of infection via dual RNA-seq analysis.Veterinary research · 2022Article
- Two-component sensor histidine kinases of Mycobacterium tuberculosis: Beacons for niche navigation.Molecular microbiology · 2022Review
- Article
- Article
- Role of the PE/PPE Family in Host-Pathogen Interactions and Prospects for Anti-Tuberculosis Vaccine and Diagnostic Tool Design.Frontiers in cellular and infection microbiology · 2020Review
- New insights into the mycobacterial PE and PPE proteins provide a framework for future research.Molecular microbiology · 2020Review
- Mycobacterium tuberculosis Requires Regulation of ESX-5 Secretion for Virulence in Irgm1-Deficient Mice.Infection and immunity · 2019Article
- Redox-dependent condensation of the mycobacterial nucleoid by WhiB4.Redox biology · 2018Article
- Article
- Multiplexed Quantitation of Intraphagocyte Mycobacterium tuberculosis Secreted Protein Effectors.Cell reports · 2018Article
- Chemical Genetic Interaction Profiling Reveals Determinants of Intrinsic Antibiotic Resistance in Mycobacterium tuberculosis.Antimicrobial agents and chemotherapy · 2017Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mycobacterium tuberculosis requires the phosphate-sensing signal transduction system Pst/SenX3-RegX3 to resist host immune responses. A ΔpstA1 mutant lacking a Pst phosphate uptake system component is hypersensitive to diverse stress conditions in vitro and is attenuated in vivo due to constitutive expression of the phosphate starvation-responsive RegX3 regulon. Transcriptional profiling of the ΔpstA1 mutant revealed aberrant expression of certain pe and ppe genes. PE and PPE proteins, defined by conserved N-terminal domains containing Pro-Glu (PE) or Pro-Pro-Glu (PPE) motifs, account for a substantial fraction of the M. tuberculosis genome coding capacity, but their functions are largely uncharacterized. Because some PE and PPE proteins localize to the cell wall, we hypothesized that overexpression of these proteins sensitizes M. tuberculosis to stress by altering cell wall integrity. To test this idea, we deleted pe and ppe genes that were overexpressed by ΔpstA1 bacteria. Deletion of a single pe gene, pe19, suppressed hypersensitivity of the ΔpstA1 mutant to both detergent and reactive oxygen species. Ethidium bromide uptake assays revealed increased envelope permeability of the ΔpstA1 mutant that was dependent on PE19. The replication defect of the ΔpstA1 mutant in NOS2(-/-) mice was partially reversed by deletion of pe19, suggesting that increased membrane permeability due to PE19 overexpression sensitizes M. tuberculosis to host immunity. Our data indicate that PE19, which comprises only a 99-amino-acid PE domain, has a unique role in the permeability of the M. tuberculosis envelope that is regulated to resist stresses encountered in the host.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.