Mycobacterium tuberculosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA118519 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Transcriptional profiling of SirR and manganese regulated expression of genes in Mycobacterium tuberculosis strains comparing high manganese vs. low manganese in Rv (wild type Mycobacterium tuberculosis) and ST70 (mntR mutant strain of Mycobacterium tuberculosis)
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Project description:Transcriptional profiling of SirR and manganese regulated expression of genes in Mycobacterium tuberculosis strains comparing high manganese vs. low manganese in Rv (wild type Mycobacterium tuberculosis) and ST70 (mntR mutant strain of Mycobacterium tuberculosis) Two strains each with two conditions experiment, Rv (Mycobacterium tuberculosis wild type strain) high manganese vs. low manganese and ST70 (mntR mutant strain of Mycobacterium tuberculosis) high manganese vs. low manganese. Number of biological replicates is 3 for each condition for each strain.
2015-12-08 | E-GEOD-70812 | biostudies-arrayexpress
Project description:Comparison of gene expression profile of the whiB4 mutant strain of Mycobacterium tuberculosis with the wild type Mycobacterium tuberculosis H37RV Mtb WhiB4 mutant mRNA was compared with the mRNA of wtMtb H37RV under aerobic conditons Aerbic conditions OD600 nm of 0.4, MtbWhiB4KO vs wtMtb, biological replicates: 3 wt Mtb H37RV and 3 MtbWhiB4 KO
2012-07-23 | E-GEOD-37840 | biostudies-arrayexpress
Project description:New chemotherapeutics are urgently required to control the tuberculosis pandemic fueled by the emergence of multidrug- and extensively-drug-resistant Mycobacterium tuberculosis strains and the bacterium`s catastrophic alliance with HIV. Here we describe a novel trehalose-to-α-glucan pathway in M. tuberculosis comprising four enzymatic steps mediated by TreS, Pep2, GlgB, and GlgE, identified as an essential maltosyltransferase capable of utilizing maltose 1-phosphate. Using traditional and chemical reverse genetics, we show that GlgE inactivation causes rapid death of M. tuberculosis in vitro and in mice, through self-poisoning by maltose 1-phosphate accumulation driven by a self-amplifying feedback loop promoting pleiotropic phosphosugar-induced stress responses. Moreover, this α-glucan pathway exhibited a synthetic lethal interaction with the glucosyltransferase Rv3032 involved in biosynthesis of specialized α-glucan derivatives. The unique combination of gene essentiality within a synthetic lethal pathway validates GlgE as a new class of drug targets, revealing novel synergistic mechanisms to induce death in M. tuberculosis. Transcriptional profiling was performed to characterize the lethality induced by maltose 1-phosphate accumulation. Triplicate 10 mL cultures of the conditional lethal Mtb mutant strain H37Rv Delta treS Delta glgE (pMV361::treS) and of the vector control strain H37Rv Delta treS Delta glgE (pMV361) were grown in liquid culture to log-phase in the presence of 5 mM validamycin A (VA) to suppress M1P formation. Subsequently, cells were washed to remove the inhibitor; after 48 h of starvation for VA cultures were harvested. Keywords: tuberculosis, trehalose, compound treatment design, genetic modification design, and stimulus or stress design
2010-02-24 | GSE18575 | GEO
Project description:Mass Spectrometry based Phosphoproteomics was carried out on M. tuberculosis wild type strain H37Rv and the isogenic mutant strains MtbΔdosR, MtbΔdosS, and MtbΔdosT that were cultured in aerobic as well as hypoxic conditions. During later the oxygen was gradually deprived in cultures that were kept static.
2019-08-31 | PXD015256 | JPOST Repository
Project description:Transcription profile of WT compare to sigma factor sigI deletion mutant at OD1 and OD2. This microarray is simple comparison of wild type strain of M. tuberculosis CDC1551 and its sigma factor gene deletion mutant (sigI) at OD1 and OD2, respectively.
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Project description:Transcriptional profile of esx-3 conditional mutant strain (TB79) vs its parental strain (TB38) grown in 7H9 in presence of 100ng/ml Atc for 48h
2013-06-12 | GSE47834 | GEO
Project description:New chemotherapeutics are urgently required to control the tuberculosis pandemic fueled by the emergence of multidrug- and extensively-drug-resistant Mycobacterium tuberculosis strains and the bacterium`s catastrophic alliance with HIV. Here we describe a novel trehalose-to-α-glucan pathway in M. tuberculosis comprising four enzymatic steps mediated by TreS, Pep2, GlgB, and GlgE, identified as an essential maltosyltransferase capable of utilizing maltose 1-phosphate. Using traditional and chemical reverse genetics, we show that GlgE inactivation causes rapid death of M. tuberculosis in vitro and in mice, through self-poisoning by maltose 1-phosphate accumulation driven by a self-amplifying feedback loop promoting pleiotropic phosphosugar-induced stress responses. Moreover, this α-glucan pathway exhibited a synthetic lethal interaction with the glucosyltransferase Rv3032 involved in biosynthesis of specialized α-glucan derivatives. The unique combination of gene essentiality within a synthetic lethal pathway validates GlgE as a new class of drug targets, revealing novel synergistic mechanisms to induce death in M. tuberculosis. Transcriptional profiling was performed to characterize the lethality induced by maltose 1-phosphate accumulation. Triplicate 10 mL cultures of the conditional lethal Mtb mutant strain H37Rv Delta treS Delta glgE (pMV361::treS) and of the vector control strain H37Rv Delta treS Delta glgE (pMV361) were grown in liquid culture to log-phase in the presence of 5 mM validamycin A (VA) to suppress M1P formation. Subsequently, cells were washed to remove the inhibitor; after 48 h of starvation for VA cultures were harvested. Keywords: tuberculosis, trehalose, compound treatment design, genetic modification design, and stimulus or stress design Three biological replicates with one dye-flip
2010-05-14 | E-GEOD-18575 | biostudies-arrayexpress
Project description:The purpose of this study was to discover and characterize small molecule inhibitors of the M. tuberculosis DosRST two-component regulatory pathway. The impact of three novel DosRST regulon inhibitors on gene expression was studied in wild type M. tuberculosis and a DosRS mutant strain.
2016-12-19 | GSE76566 | GEO