Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

A PhoP point mutation discriminates between the virulent H37Rv and avirulent H37Ra strains of Mycobacterium tuberculosis

ABSTRACT: To uncover mutations underlying the attentuation of H37Ra, we embarked on sequencing its genome using a novel massive parallel pyrosequencing technology. Comparison with the virulent H37Rv parental strain revealed only few polymorphisms, one of which was located in the DNA binding domain of the transcriptional regulator PhoP. Keywords: Expresion profiling

OTHER RELATED OMICS DATASETS IN: PRJNA99369

ORGANISM(S): Mycobacterium tuberculosis Mycobacterium tuberculosis H37Rv Mycobacterium tuberculosis H37Ra

PROVIDER: GSE7539 | GEO | 2007/07/05

SECONDARY ACCESSION(S): PRJNA99369

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Similar Datasets

A PhoP point mutation discriminates between the virulent H37Rv and avirulent H37Ra strains of Mycobacterium tuberculosis

Project description:A PhoP point mutation discriminates between the virulent H37Rv and avirulent H37Ra strains of Mycobacterium tuberculosis

| PRJNA99369 | ENA

Quantitative proteomic and phosphoproteomic analysis of H37Ra and H37Rv strains of Mycobacterium tuberculosis

Project description:Mycobacterium tuberculosis, the causative agent of tuberculosis accounts for 1.5 million annual deaths worldwide. The two well-characterized strains of the parental H37 strain namely, H37Ra and H37Rv show different pathogenic phenotypes. In order to identify factors that are responsible for virulence, we compared the proteome and the phosphoproteome profiles of virulent (H37Rv) and virulence attenuated (H37Ra) strains of M. tuberculosis. Quantitative proteomic analysis resulted in the identification and quantitation of 2,709 proteins and 505 phosphosites. Comparative analysis revealed over 5-fold overexpression of several proteins associated with virulence. Our data indicates that there are definable molecular differences between H37Rv and H37Ra strains at both the proteome and phosphoproteome levels which may explain the virulence and phenotypic differences.

2017-05-08 | PXD004161 | Pride

proteomics analysis of virulent and avirulent strains of mycobacterium

Project description:label free quantification analysis was performed on four strains of mycobacterium tuberculosis. The four strains are H37Rv, H37Ra, BND and JAL. The purpose of this study is to identify strain specific proteome expression pattern among the four strains.

2016-05-10 | PXD001188 | Pride

LIX48 (H37Ra-devR overexpression) versus LIX47 (control strain) and LIX50 (H37Rv-devR overexpression) versus LIX49 (control strain)

Project description:Transcription analysis of M. tuberculosis H37Ra devR overexpressing strain (LIX48) versus empty vector control strain (LIX47); H37Rv devR overexpressing strain t (LIX50) versus empty vector control strain (LIX49) to study the effect of DevR overexpression

2018-08-31 | GSE103551 | GEO

PBMCs exposed to the Mycobacterium tuberculosis H37Ra strain

Project description:Human peripheral blood mononuclear cells were cultured in presence of H37Ra strain at 37oC, 5%CO2. Cellular aggregates were collected at 24h, and RNA extracted and hybridized to Affymetrix microarrays (HG-U133). Raw data from microarray experiments was analyzed with dCHIP and SAM programs to determine the significance of changes at the biological context. PBMCs were exposed in triplicate to H37Ra strain. PBMCs from the same donor were cultured in triplicate at the same conditions than treated samples. RNA was extracted from each sample and hybridized to Affymetrix Human arrays.

2014-05-28 | E-GEOD-16250 | biostudies-arrayexpress

M. tuberculosis phoP mutant lacking mcr7

Project description:The PhoPR two-component system is essential for virulence in Mycobacterium tuberculosis where it controls expression of approximately 2% of the genes, including those for the ESX-1 secretion apparatus, a major virulence determinant. Mutations in phoP lead to compromised production of pathogen-specific cell wall components and attenuation both ex vivo and in vivo. The PhoP regulon comprises several transcriptional regulators as well as genes for polyketide synthases and PE/PPE proteins. The most prominent site of PhoP regulation was located in the intergenic region between rv2395 and PE_PGRS41, where the mcr7 gene codes for a small non-coding RNA (ncRNA). Our prediction suggested that Mcr7 might regulate tatC at the post-transcriptional level by occlusion of the RBS and the consequent translational arrest. Consequently, we studied the secretome from exponentially grown cultures of strain H37Rv, its phoP mutant and a phoP complemented mutant by in-depth proteomics. The results are consistent with a regulatory model involving PhoP, Mcr7 and tatC mRNA since the absence of Mcr7 in the phoP mutant would result in more efficient TatC translation and therefore increased secretion.

2018-08-29 | PXD000698 | Pride

PhoP regulon in pathogenic Escherichia coli

Project description:PhoP is considered a regulator of virulence despite being conserved in both pathogenic and non-pathogenic Enterobacteriaceae. While Escherichia coli strains represent both non-pathogenic commensal isolates and numerous virulent pathotypes, the PhoP virulence regulator has only been studied in commensal E. coli. To better understand how conserved transcription factors contribute to virulence, we characterized PhoP in pathogenic E. coli. Loss of phoP significantly attenuated E. coli during extraintestinal infection. This was not surprising since we demonstrated that PhoP differentially regulated the transcription of >600 genes. In addition to survival at acidic pH and resistance to polymyxin B, PhoP was required for repression of motility and oxygen-independent changes in the expression of primary dehydrogenase and terminal reductase respiratory chain components. All phenotypes have in common a reliance on an energized membrane. Thus, we hypothesized that PhoP mediated these effects by regulating genes that generate a proton motive force. Indeed, bacteria lacking PhoP exhibited a hyper-polarized membrane, and dissipation of the transmembrane electrochemical gradient increased the susceptibility of the phoP mutant to acidic pH, while inhibiting respiratory generation of the proton gradient restored resistance to antimicrobial peptides independent of lipopolysaccharide modification. These findings demonstrate a connection between PhoP, virulence, and the energized state of the membrane.

2011-07-29 | GSE31029 | GEO

Comparative transcriptomic analysis of THP‑1 derived macrophages infected with Mycobacterium tuberculosis H37Rv, H37Ra and BCG

Project description:In this study, RNA sequencing (Transcriptome sequencing) was employed to investigate the global transcriptome changes in the macrophages during the different strains of M.tb infection. THP-1 cells derived macrophages were exposed to the virulent M.tb strain H37Rv (Rv) or the avirulent M.tb strain H37Ra (Ra), and the M.tb BCG vaccine strain was used as a control. The cDNA libraries were prepared from M.tb infected macrophages and then sequenced.

2020-12-06 | GSE162729 | GEO

Real-time quantitative PCR analysis of PMA differentiated THP-1 infected with H37Rv or M. marinum, or heat killed H37Ra (HKMT)

Project description:THP-1 cells were differentiated into macrophages with 0,1 µM PMA overnight then infected for 2 days with either H37Rv, M. marinum or heat killed H37Ra. Then RNA was collected in order to quantify the inflammatory response transcription as compared with the relative uninfected controls.

2021-07-20 | GSE165327 | GEO

Transcription profiling of Yersinia pestis overexpressing phoP

Project description:Microarrays were used to identify Y. pestis genes that are differentially regulated under conditions of phoP overexpression. RNA samples were isolated from cultures of two isogenic Y. pestis strains, one overexpressing phoP (KIM10+phoP(delta)/PhoP) and the other not (KIM10+phoP(delta)/MMB67EH), and their gene expression profiles were compared.

2006-07-01 | E-MEXP-712 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

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