Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Transcriptional response of Mycobacterium tuberculosis ΔlucA::hyg and complemented strains vs. WT in resting murine bone marrow-derived macrophages

ABSTRACT: Transcriptional response of Mycobacterium tuberculosis ΔlucA::hyg mutant and complemented strains vs. WT in resting murine bone marrow-derived macrophages was analyzed in this study. This data demonstrates that deletion of lucA leads to perturbed expression of the genes linked to fatty acid and cholesterol metabolism of the pathogen during macrophage infection. It supports an overall conclusion of the publication that LucA serves an important role in function of fatty acid and choletserol transporters.

ORGANISM(S): Mycobacterium tuberculosis

PROVIDER: GSE98792 | GEO | 2017/05/22

SECONDARY ACCESSION(S): PRJNA386249

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

TraSH analysis of Mycobacterium tuberculosis transposon mutants with reduced bodipy-palmitate uptake on the third day of resting bone marrow-derived macrophage infection

Project description:Mycobacterium tuberculosis transposon mutants with reduced bodipy-palmitate intake on the third day of resting bone marrow-derived macrophage infection are identified by TraSH. Discovery of genetic requirements for fatty acid assimilation by the pathogen is essential for understanding its metabolism during host infection.

2018-11-30 | GSE119753 | GEO

Intracellular transcriptional adaptation of Mycobacterium tuberculosis complex (MTC) clinical isolates inside resting murine macrophages

Project description:This study uses microarray analyses to examine transcriptional responses of Mycobacterium tuberculosis complex clinical isolates to phagosomal cues encountered inside resting murine bone marrow-derived macrophages 24hr post-infection. Transcript levels of intracellular mycobacteria were compared to extracellular bacteria of the same strain (An aliquot of the inoculum used to infect macrophages was incubated in the absence of macrophages for 24hr in an identical flask). Set of arrays that are part of repeated experiments Keywords: Biological Replicate

2010-07-09 | GSE21112 | GEO

Intracellular transcriptional adaptation of Mycobacterium tuberculosis complex (MTC) clinical isolates inside resting murine macrophages

2010-07-09 | E-GEOD-21112 | biostudies-arrayexpress

Transcriptomic analysis of untreated log-phase Mtb H37Rv, Mtbrv0158 Knockout strain and Mtbrv0158 complemented strain

Project description:We identified rv0158 gene as a major determinant of redox homeostasis in Mtb. Disruption of rv0158 perturbed redox balance in a carbon source-specific manner, promoted killing in response to anti-TB drugs, reduced survival in macrophages, and persistence in mice. RNA sequencing analysis was performed to identify its regulon. The data indicated that rv0158 is required to balance the deployment of fatty acid substrates between lipid anabolism and oxidation.

2023-09-04 | GSE196844 | GEO

Sequence analysis of Mycobacterium tuberculosis

Project description:Study to perform RNAseq on the Mtb ?esx3 and complemented control including the non-coding RNAs.These data are part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

2015-06-23 | E-ERAD-355 | biostudies-arrayexpress

Mycobacterium transcription survey

Project description:Study on correlation between methylation and transcription patterns in Mycobacterium tuberculosis strains.These data are part of a pre-publication release. For information on the proper use of pre-publication data shared by the Wellcome Trust Sanger Institute (including details of any publication moratoria), please see http://www.sanger.ac.uk/datasharing/

2015-11-17 | E-ERAD-409 | biostudies-arrayexpress

Resting CD4+ T cells exposed to oleic acid upregulate genes involved in immunometabolism resulting in increased IL-9+ frequencies post-activation [DNA methylation]

Project description:T cells are the most common immune cell in atherosclerotic plaques. Furthermore, T cell function is influenced by fatty acids that are abundant in the circulation and atherosclerotic plaques. Here, we define the effect of oleic acid, one of the most abundant fatty acids in the human circulation, on the transcriptome of resting CD4+ T cells and subsequently the polarization of the cells into T cell subsets post-activation. We first performed RNA sequencing of resting CD4+ T cells from 9 donors after 0.5, 3, 24, 48, and 72 hours exposure to 30µg/mL oleic acid. This revealed the upregulation of genes involved in cholesterol biosynthesis (HMGCR, SQLE, MVD and MVK) and de novo fatty acid biosynthesis (ACACA and FASN). Both pathways point to a metabolic reprogramming of the cells towards a pro-inflammatory state. Subsequently, a 26-marker spectral flow cytometry panel showed increased frequencies of IL-9+ and IL-17A+ cells among activated CD4+ T cells pre-exposed to oleic acid. IL-9 and IL-17A are primarily produced by the respective T helper (TH) subsets TH9 and TH17, where, especially TH9, has been implicated in the aggravation of atherosclerosis. Our data shows that oleic acid may induce a shift in immunometabolism in resting CD4+ T cells towards an activated profile that leads to more pro-inflammatory and pro-atherogenic polarization of these cells post-activation. Taken together, our study signals a potential role for the interaction between circulating fatty acids and CD4+ T cells in the development and pathogenesis of atherosclerosis.

2024-02-13 | GSE231457 | GEO

Resting CD4+ T cells exposed to oleic acid upregulate genes involved in immunometabolism resulting in increased IL-9+ frequencies post-activation [RNA-seq]

2024-02-13 | GSE231458 | GEO

Mycobacterium tuberculosis

Project description:Transcriptional response of Mycobacterium tuberculosis ΔlucA::hyg and complemented strains vs. WT in resting murine bone marrow-derived macrophages

| PRJNA386249 | ENA

Transcription profiling of Mycobacterium tuberculosis wild type, ideR mutant and ideR complemented mutants strains grown in iron-sufficient or iron-deficient media

Project description:The mycobacterial IdeR protein is a metal-dependent regulator of the DtxR (diphtheria toxin repressor) family. In the presence of iron, it binds to a specific DNA sequence in the promoter regions of the genes that it regulates, thus controlling their transcription. In this study, we provide evidence that ideR is an essential gene in Mycobacterium tuberculosis. ideR cannot normally be disrupted in this mycobacterium in the absence of a second functional copy of the gene. However, a rare ideR mutant was obtained in which the lethal effects of ideR inactivation were alleviated by a second-site suppressor mutation and which exhibited restricted iron assimilation capacity. Studies of this strain and a derivative in which IdeR expression was restored allowed us to identify phenotypic effects resulting from ideR inactivation. Using DNA microarrays, the iron-dependent transcriptional profiles of the wild-type, ideR mutant, and ideR complemented mutant strains were analyzed, and the genes regulated by iron and IdeR were identified. These genes encode a variety of proteins, including putative transporters, proteins involved in siderophore synthesis and iron storage, members of the PE/PPE family, a membrane protein involved in virulence, transcriptional regulators, and enzymes involved in lipid metabolism.

2007-09-12 | E-TABM-317 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data