Mycobacterium tuberculosis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA113869 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:This SuperSeries is composed of the following subset Series: GSE11696: Gene expression profile of M.tuberculosis espR (Rv3849) mutant GSE12379: Gene expression profile of M.tuberculosis espR (Rv3849) mutant complemented with an N-terminal Flag espR gene GSE12380: Gene expression profile of M.tuberculosis espR (Rv3849) mutants containing N- or C-terminal mutations in the espR gene GSE12381: Comparative analysis of the gene expression profiles of M.tuberculosis espR (Rv3849) transposon and knockout mutants Refer to individual Series
2010-05-25 | E-GEOD-12382 | biostudies-arrayexpress
Project description:Gene expression profile of M.tuberculosis espR (Rv3849) mutants containing N- or C-terminal mutations in the espR gene
| PRJNA113867 | ENA
Project description:Gene expression profile of M.tuberculosis espR (Rv3849) mutant
| PRJNA113825 | ENA
Project description:Gene expression profile of M.tuberculosis espR (Rv3849) mutant complemented with an N-terminal Flag espR gene
| PRJNA113865 | ENA
Project description:The principal virulence determinant of Mycobacterium tuberculosis (Mtb), the ESX-1 protein secretion system, is positively controlled at the transcriptional level by EspR. Depletion of EspR reportedly affects a small number of genes, both positively or negatively, including a key ESX-1 component, the espACD operon. EspR is also thought to be an ESX-1 substrate. Using EspR-specific antibodies in ChIP-Seq experiments (chromatin immunoprecipitation followed by ultra-high throughput DNA sequencing) we show that EspR binds to at least 165 loci on the Mtb genome. Included in the EspR regulon are genes encoding not only EspA, but also EspR itself, the ESX-2 and ESX-5 systems, a host of diverse cell wall functions, such as production of the complex lipid PDIM (phenolthiocerol dimycocerosate) and the PE/PPE cell-surface proteins. EspR binding sites are not restricted to promoter regions and can be clustered. This suggests that rather than functioning as a classical regulatory protein EspR acts globally as a nucleoid-associated protein capable of long-range interactions consistent with a recently established structural model. EspR expression was shown to be growth phase-dependent, peaking in the stationary phase. Overexpression in Mtb strain H37Rv revealed that EspR influences target gene expression both positively or negatively leading to growth arrest. At no stage was EspR secreted into the culture filtrate. Thus, rather than serving as a specific activator of a virulence locus, EspR is a novel nucleoid-associated protein, with both architectural and regulatory roles, that impacts cell wall functions and pathogenesis through multiple genes.
2012-04-02 | GSE35149 | GEO
Project description:The principal virulence determinant of Mycobacterium tuberculosis (Mtb), the ESX-1 protein secretion system, is positively controlled at the transcriptional level by EspR. Depletion of EspR reportedly affects a small number of genes, both positively or negatively, including a key ESX-1 component, the espACD operon. EspR is also thought to be an ESX-1 substrate. Using EspR-specific antibodies in ChIP-Seq experiments (chromatin immunoprecipitation followed by ultra-high throughput DNA sequencing) we show that EspR binds to at least 165 loci on the Mtb genome. Included in the EspR regulon are genes encoding not only EspA, but also EspR itself, the ESX-2 and ESX-5 systems, a host of diverse cell wall functions, such as production of the complex lipid PDIM (phenolthiocerol dimycocerosate) and the PE/PPE cell-surface proteins. EspR binding sites are not restricted to promoter regions and can be clustered. This suggests that rather than functioning as a classical regulatory protein EspR acts globally as a nucleoid-associated protein capable of long-range interactions consistent with a recently established structural model. EspR expression was shown to be growth phase-dependent, peaking in the stationary phase. Overexpression in Mtb strain H37Rv revealed that EspR influences target gene expression both positively or negatively leading to growth arrest. At no stage was EspR secreted into the culture filtrate. Thus, rather than serving as a specific activator of a virulence locus, EspR is a novel nucleoid-associated protein, with both architectural and regulatory roles, that impacts cell wall functions and pathogenesis through multiple genes. ChIP-Seq of EspR in Mtb H37Rv at mid-log phase of growth. Two independent experiments were performed. Input DNA (No IP) was used as a control.
2012-04-02 | E-GEOD-35149 | biostudies-arrayexpress
Project description:We investigated transcriptional responses of different lung macrophage lineages during M.tuberculosis infection by RNAseq. Our data revealed that different lineages of macrophages respond differentially to M.Tuberculosis infection.
2018-02-21 | GSE108844 | GEO
Project description:The genome wide transcriptome analysis to identify the M.tuberculosis sigma factor Rv3286c (SigF) dependent transcripts as well as Pristimaycin induced transcripts
2012-01-20 | GSE34922 | GEO
Project description:The genome wide ChIP-on-chip analysis to identify the DNA binding sites for the M.tuberculosis sigma factor Rv3286c (SigF)
2012-01-20 | GSE34919 | GEO
Project description:Background: M.tuberculosis is one of the most prevalent and deadly human pathogens. The molecular mechanisms determining the outcomes of an infection with M.tuberculosis, that range from resistance to an active progressive disease, remain incompletely understood. Here we provide the evidence that IL-1alpha plays a critical and non-redundant role in enabling host resistance to pulmonary M.tuberculosis infection in mice that develop functional pathogen-specific adaptive immunity. Mechanistically, IL-1alpha-deficient mice fail to control M.tuberculosis replication in vivo at a level of individual infected cells and succumb to progressive disease at the late phase of infection. Furthermore, we show that IL-1alpha from hematopoietic compartment through IL-1RI operates upstream of TNFRI-signaling pathway and the lack of IL-1alpha leads to the continuous influx of monocytes that acquire a hyper-inflammatory phenotype and contribute to pathology, rather than to a pathogen control. Cell-type-specific restoration of IL-1alpha expression in CD11c+ subsets of lung leukocytes resulted in reduced levels of inflammatory marker expression on lung cells and improved survival IL-1alpha-deficient mice after M.tuberculosis infection. In humans, genetic analysis of single nucleotide polymorphisms in 14 genes implicated in IL-1-IL-1R signaling pathway revealed association of genetic variations in IL-1alpha and IL-1RAP genes with human susceptibility to pulmonary tuberculosis. Our results implicate IL-1alpha as a principal factor of host resistance to M.tuberculosis and IL-1alpha-driven cell-cell crosstalk as a key step in triggering M.tuberculosis control mechanisms that are critical for host survival.
2019-09-03 | GSE32619 | GEO