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A validated microarray platform for Mycobacterium tuberculosis

ABSTRACT: The new microarray described for Mycobacterium tuberculosis in our study has a more complete reprensentation of the genome than any other array design reported till date. Further, protocols for sample preparation, labelling and hybridisation for accurate gene expression profiling of M.tuberculosis have been optimised.

ORGANISM(S): Mycobacterium tuberculosis H37Rv

PROVIDER: GSE45811 | GEO | 2013/06/01

SECONDARY ACCESSION(S): PRJNA196407

REPOSITORIES: GEO

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A validated microarray platform for Mycobacterium tuberculosis

Project description:The new microarray described for Mycobacterium tuberculosis in our study has a more complete reprensentation of the genome than any other array design reported till date. Further, protocols for sample preparation, labelling and hybridisation for accurate gene expression profiling of M.tuberculosis have been optimised. Whole genome expression profiling on Mycobacterium tuberculosis H37Rv (OD600 0.4-0.5) was performed using exponential phase cultures after 0 and 6 Hrs in presence and absence of drug (Isoniazid) by using PolyA-dT and WT method. The exponential culture after 24 and 72 Hrs were used for validating the specific hybridization with or without formamide. All time points had two biological replicates with two technical replicates.

2013-06-01 | E-GEOD-45811 | biostudies-arrayexpress

Mycobacterium tuberculosis whole cell lysates

Project description:Proteomics on whole cell lysates from Mycobacterium tuberculosis CDC1551, a ppe38-ppe71 deletion mutant and a complemented strain grown in modified sautons medium till mid logarithmic phase

2021-06-15 | PXD020814 | Pride

Secreted transcription factor controls Mycobacterium tuberculosis virulence

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

Transcriptional profiles of lung macrophage subsets in Mycobacterium Tuberculosis infection

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

RNA sequencing of neutrophils isolated from lung, spleen and bone marrow of Mycobacterium tuberculosis infected mice

Project description:Mycobacterium tuberculosis infection of mice elicits a robust neutrophil influx that associates with poor outcome from tuberculosis (TB). However, the mechanism by which neutrophils contribute to TB disease pathogenesis is not understood. To gain insights into the pathological functions of neutrophils, the current study performs bulk mRNA sequencing from the neutrophils isolated from lung, spleen and bone marrow of resistant (C57BL/6) and susceptible (IL-1R1 KO) mice at 28 days post M.tuberculosis HN878 infection.

2024-02-29 | GSE203118 | GEO

Transcriptional response of Mycobacterium tuberculosis in mouse peritoneal neutrophils

Project description:This study was conducted to descripe transcriptomic changes of M.tuberculosis during neutrophil infection

2019-11-09 | GSE140156 | GEO

Dissection of the heat-shock response in Mycobacterium tuberculosis using mutants and microarrays

Project description:Regulation of the expression of heat-shock proteins plays an important role in the pathogenesis of Mycobacterium tuberculosis. The heat-shock response of bacteria involves genome-wide changes in gene expression. A combination of targeted mutagenesis and whole-genome expression profiling was used to characterize transcription factors responsible for control of genes encoding the major heat-shock proteins of M.tuberculosis. Two heat-shock regulons were identified. HspR acts as a transcriptional repressor for the members of the Hsp70 (DnaK) regulon, and HrcA similarly regulates the Hsp60 (GroE)response. These two specific repressor circuits overlap with broader transcriptional changes mediated by alternative sigma factors during exposure to high temperatures. Several previously undescribed heat-shock genes were identified as members of the HspR and HrcA regulons. A novel HspR-controlled operon encodes a member of the low-molecular-mass a-crystallin family. This protein is one of the most prominent features of the M.tuberculosis heatshock response and is related to a major antigen induced in response to anaerobic stress. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-2

2007-03-07 | E-BUGS-2 | biostudies-arrayexpress

Response of M. tuberculosis to 8 hour exposure to vitamin C

Project description:Transcriptional profiling of M.tuberculosis to 10 mM vitamin C at 8 h. This was compared to gene expression profile of untreated M. tuberculosis culture. Organism: Mycobacterium tuberculosis H37Rv, Genotypic Technology designed Custom Mycobacterium tuberculosis H37Rv Whole Genome 8x15k GE Microarray (AMADID-020181)

2014-10-01 | E-GEOD-60376 | biostudies-arrayexpress

Host resistance to pulmonary infection with Mycobacterium tuberculosis is mediated by IL-1alpha.

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

Microarray analysis of defined Mycobacterium tuberculosis populations using RNA amplification strategies

Project description:Background The amplification of bacterial RNA is required if complex host-pathogen interactions are to be studied where the recovery of bacterial RNA is limited. Here, using a whole genome Mycobacterium tuberculosis microarray to measure cross-genome representation of amplified mRNA populations, we have investigated two approaches to RNA amplification using different priming strategies. The first using oligo-dT primers after polyadenylation of the bacterial RNA, the second using a set of mycobacterial amplification-directed primers. Results The reproducibility, sensitivity, and the representational bias introduced by these amplification systems were examined by contrasting expression profiles of the amplified products from inputs of 500, 50 and 5ng total M.tuberculosis RNA with unamplified RNA from the same source. In addition a model M.tuberculosis system of microaerophilic growth and non-replicating persistence was used to assess the capability of amplified RNA microarray comparisons from an experimental system where RNA yield is restricted. Mycobacterial RNA was reproducibly amplified using both methods from as little as 5ng total RNA (~ equivalent to 2E+05 bacilli). Differential gene expression patterns observed with unamplified RNA in the switch from aerobic to microaerophilic growth were also reflected in the amplified expression profiles. Conclusions Here we describe two reproducible methods of bacterial RNA amplification that will allow previously intractable host-pathogen interactions during bacterial infection to be explored at the whole genome level by RNA profiling. Data is also available from http://bugs.sgul.ac.uk/E-BUGS-42

2008-03-12 | E-BUGS-42 | biostudies-arrayexpress

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