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Mycobacterium tuberculosis produces small noncoding RNAs that support mycobacterial survival in infected cells [RNA-seq]

ABSTRACT: The purpose of this study was to identify the role of sncRNA-1 using a gain of function approach. It was overexpressed in 3 clones and Total RNA was sequenced in 3 clones that had either the ctl vector or the sncRNA-1 vector. Differentially expressed genes were analyzed.

ORGANISM(S): Mycobacterium tuberculosis

PROVIDER: GSE146227 | GEO | 2020/03/03

REPOSITORIES: GEO

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Mycobacterium tuberculosis produces small noncoding RNAs that support mycobacterial survival in infected cells

Project description:This SuperSeries is composed of the SubSeries listed below.

2020-03-03 | GSE146228 | GEO

Mycobacterium tuberculosis produces small noncoding RNAs that support mycobacterial survival in infected cells [miRNA discovery screen]

Project description:The purpose of this study was to identify Mtb- and hsa-encoded miRNAs produced in infected macrophages. RNA from 9 THP-1 samples (3 were uninfected, 3 were infected with Mtb H37Rv for 3 days and 3 were infected with Mtb H37Rv for 6 days) was sequenced and miRNAs were detected.

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Mycobacterium tuberculosis produces small noncoding RNAs that support mycobacterial survival in infected cells

Project description:Mycobacterium tuberculosis produces small noncoding RNAs that support mycobacterial survival in infected cells

| PRJNA609737 | ENA

Mycobacterium tuberculosis produces small noncoding RNAs that support mycobacterial survival in infected cells [RNA-seq]

Project description:Mycobacterium tuberculosis produces small noncoding RNAs that support mycobacterial survival in infected cells [RNA-seq]

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Mycobacterial DNA binding protein 1 (MDP1) mediates gene regulation in Mycobacterium tuberculosis variant Bacillus Calmette-Guerin

Project description:To investigate the role of MDP1 in global transcription regulation, we established MDP1 conditional knockdown BCG using CRISPR/dCas9 system. Transcriptome profiling was then performed using data obtained from RNA-seq of two BCG MDP1 mutants compared to the vector control at three growth time points.

2023-08-01 | GSE222247 | GEO

Mycobacterium tuberculosis produces small noncoding RNAs that support mycobacterial survival in infected cells [miRNA discovery screen]

Project description:Mycobacterium tuberculosis produces small noncoding RNAs that support mycobacterial survival in infected cells [miRNA discovery screen]

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Mycobacterium tuberculosis produces pili during human infection.

Project description:Mycobacterium tuberculosis is responsible for nearly 3 million human deaths worldwide every year. Understanding the mechanisms and bacterial factors responsible for the ability of M. tuberculosis to cause disease in humans is critical for the development of improved treatment strategies. Many bacterial pathogens use pili as adherence factors to colonize the host. We discovered that M. tuberculosis produces fine (2- to 3-nm-wide), aggregative, flexible pili that are recognized by IgG antibodies contained in sera obtained from patients with active tuberculosis, indicating that the bacilli produce pili or pili-associated antigen during human infection. Purified M. tuberculosis pili (MTP) are composed of low-molecular-weight protein subunits encoded by the predicted M. tuberculosis H37Rv ORF, designated Rv3312A. MTP bind to the extracellular matrix protein laminin in vitro, suggesting that MTP possess adhesive properties. Isogenic mtp mutants lost the ability to produce Mtp in vitro and demonstrated decreased laminin-binding capabilities. MTP shares morphological, biochemical, and functional properties attributed to bacterial pili, especially with curli amyloid fibers. Thus, we propose that MTP are previously unidentified host-colonization factors of M. tuberculosis.

| S-EPMC1817835 | biostudies-literature

Crystal structure of Mycobacterium tuberculosis FadB2 implicated in mycobacterial ?-oxidation.

Project description:The intracellular pathogen Mycobacterium tuberculosis is the causative agent of tuberculosis, which is a leading cause of mortality worldwide. The survival of M. tuberculosis in host macrophages through long-lasting periods of persistence depends, in part, on breaking down host cell lipids as a carbon source. The critical role of fatty-acid catabolism in this organism is underscored by the extensive redundancy of the genes implicated in ?-oxidation (?100 genes). In a previous study, the enzymology of the M. tuberculosis L-3-hydroxyacyl-CoA dehydrogenase FadB2 was characterized. Here, the crystal structure of this enzyme in a ligand-free form is reported at 2.1?Å resolution. FadB2 crystallized as a dimer with three unique dimer copies per asymmetric unit. The structure of the monomer reveals a dual Rossmann-fold motif in the N-terminal domain, while the helical C-terminal domain mediates dimer formation. Comparison with the CoA- and NAD+-bound human orthologue mitochondrial hydroxyacyl-CoA dehydrogenase shows extensive conservation of the residues that mediate substrate and cofactor binding. Superposition with the multi-catalytic homologue M. tuberculosis FadB, which forms a trifunctional complex with the thiolase FadA, indicates that FadB has developed structural features that prevent its self-association as a dimer. Conversely, FadB2 is unable to substitute for FadB in the tetrameric FadA-FadB complex as it lacks the N-terminal hydratase domain of FadB. Instead, FadB2 may functionally (or physically) associate with the enoyl-CoA hydratase EchA8 and the thiolases FadA2, FadA3, FadA4 or FadA6 as suggested by interrogation of the STRING protein-network database.

| S-EPMC6333283 | biostudies-literature

Mycobacterium tuberculosis Zinc Metalloprotease-1 Assists Mycobacterial Dissemination in Zebrafish.

Project description:Zinc metalloprotease-1 (Zmp1) from Mycobacterium tuberculosis (M.tb), the tuberculosis (TB) causing bacillus, is a virulence factor involved in inflammasome inactivation and phagosome maturation arrest. We earlier reported that Zmp1 was secreted under granuloma-like stress conditions, induced Th2 cytokine microenvironment and was highly immunogenic in TB patients as evident from high anti-Zmp1 antibody titers in their sera. In this study, we deciphered a new physiological role of Zmp1 in mycobacterial dissemination. Exogenous treatment of THP-1 cells with 500 nM and 1 ?M of recombinant Zmp1 (rZmp1) resulted in necrotic cell death. Apart from inducing secretion of necrotic cytokines, TNF?, IL-6, and IL-1?, it also induced the release of chemotactic chemokines, MCP-1, MIP-1?, and IL-8, suggesting its likely function in cell migration and mycobacterial dissemination. This was confirmed by Gap closure and Boyden chamber assays, where Zmp1 treated CHO or THP-1 cells showed ?2 fold increased cell migration compared to the untreated cells. Additionally, Zebrafish-M. marinum based host-pathogen model was used to study mycobacterial dissemination in vivo. Td-Tomato labeled M. marinum (TdM. marinum) when injected with rZmp1 showed increased dissemination to tail region from the site of injection as compared to the untreated control fish in a dose-dependent manner. Summing up these observations along with the earlier reports, we propose that Zmp1, a multi-faceted protein, when released by mycobacteria in granuloma, may lead to necrotic cell damage and release of chemotactic chemokines by surrounding infected macrophages, attracting new immune cells, which in turn may lead to fresh cellular infections, thus assisting mycobacterial dissemination.

| S-EPMC5002425 | biostudies-literature

Phase variation in Mycobacterium tuberculosis glpK produces transiently heritable drug tolerance.

Project description:The length and complexity of tuberculosis (TB) therapy, as well as the propensity of Mycobacterium tuberculosis to develop drug resistance, are major barriers to global TB control efforts. M. tuberculosis is known to have the ability to enter into a drug-tolerant state, which may explain many of these impediments to TB treatment. We have identified a mechanism of genetically encoded but rapidly reversible drug tolerance in M. tuberculosis caused by transient frameshift mutations in a homopolymeric tract (HT) of 7 cytosines (7C) in the glpK gene. Inactivating frameshift mutations associated with the 7C HT in glpK produce small colonies that exhibit heritable multidrug increases in minimal inhibitory concentrations and decreases in drug-dependent killing; however, reversion back to a fully drug-susceptible large-colony phenotype occurs rapidly through the introduction of additional insertions or deletions in the same glpK HT region. These reversible frameshift mutations in the 7C HT of M. tuberculosis glpK occur in clinical isolates, accumulate in M. tuberculosis-infected mice with further accumulation during drug treatment, and exhibit a reversible transcriptional profile including induction of dosR and sigH and repression of kstR regulons, similar to that observed in other in vitro models of M. tuberculosis tolerance. These results suggest that GlpK phase variation may contribute to drug tolerance, treatment failure, and relapse in human TB. Drugs effective against phase-variant M. tuberculosis may hasten TB treatment and improve cure rates.

| S-EPMC6765255 | biostudies-literature

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