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Initial host response to mycobacterial infection is orchestrated through H3K4 methylation-mediated RNA polymerase II binding at key immune function genes [RNA-seq]

ABSTRACT: Massive reprogramming of the host alveolar macrophage transcriptome occurs during the initial stages of tuberculosis. In bovine tuberculosis, Mcobacterium bovis can persist and replicate within alveolar macrophages through varied mechanisms to subvert or exploit host immune responses ( REF). To determine how these transcriptional changes are regulated we performed ChIPseq analysis of H3K4 and H3K27 methylation, established histone tail markers associated with permissive and repressive chromatin states, respectively. These analyses were carried out in parallel with RNA polymerase II ChIPseq, RNAseq and small non-coding RNAseq. This meta data file refers to the RNA-seq datasets.

ORGANISM(S): Bos taurus

PROVIDER: GSE116732 | GEO | 2019/07/05

REPOSITORIES: GEO

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Initial host response to mycobacterial infection is orchestrated through H3K4 methylation-mediated RNA polymerase II binding at key immune function genes [miRNA-seq]

Project description:Massive reprogramming of the host alveolar macrophage transcriptome occurs during the initial stages of tuberculosis. In bovine tuberculosis, Mcobacterium bovis can persist and replicate within alveolar macrophages through varied mechanisms to subvert or exploit host immune responses ( REF). To determine how these transcriptional changes are regulated we performed ChIPseq analysis of H3K4 and H3K27 methylation, established histone tail markers associated with permissive and repressive chromatin states, respectively. These analyses were carried out in parallel with RNA polymerase II ChIPseq, RNAseq and small non-coding RNAseq. This meta data file refers to the miRNA-seq datasets.

2019-07-05 | GSE116733 | GEO

Initial host response to mycobacterial infection is orchestrated through H3K4 methylation-mediated RNA polymerase II binding at key immune function genes [ChIP-seq]

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Secretome Analysis of Mycobacterial-infected Bovine Macrophages

Project description:Mycobacterium tuberculosis (Mtb) is the causative agent of tuberculosis, a chronic granulomatous disease. Mtb is mostly restricted to humans and seldom causes disease in animals. M. bovis (Mbv) on the other hand causes tuberculosis in cows (bovine tuberculosis) and several wild animals. Each of these pathogens therefore has unique host adaptations and the host- and pathogen-specific factors driving this differential tropism still remain largely unknown. Here we profiled the secretomes of Mtb- and Mbv-infected bovine macrophages to characterise host-specific responses to each pathogen.

2021-03-11 | PXD017949 | Pride

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Project description:In this study we have used ChIPseq analysis to perform comprehensive mapping of the binding profile of the cAMP receptor protein (CRPMt) of M. tuberculosis combined with RNAseq studies to further investigate the transcriptional response following crp gene deletion and under alternative growth conditions.

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Project description:Mycobacterium tuberculosis thrives within macrophages by residing in phagosomes and preventing them from maturing and fusing with lysosomes. A parallel transcriptional survey of intracellular mycobacteria and their host macrophages revealed signatures of heavy metal poisoning. In particular, mycobacterial genes encoding heavy metal efflux P-type ATPases CtpC, CtpG, and CtpV, and host cell metallothioneins and zinc exporter ZnT1, were induced during infection. Consistent with this pattern of gene modulation, we observed a burst of free zinc inside macrophages, and intraphagosomal zinc accumulation within a few hours postinfection. Zinc exposure led to rapid CtpC induction, and ctpC deficiency caused zinc retention within the mycobacterial cytoplasm, leading to impaired intracellular growth of the bacilli. Thus, the use of P(1)-type ATPases represents a M. tuberculosis strategy to neutralize the toxic effects of zinc in macrophages. We propose that heavy metal toxicity and its counteraction might represent yet another chapter in the host-microbe arms race. [Data is also available from http://bugs.sgul.ac.uk/E-BUGS-122]

2012-01-27 | E-BUGS-122 | biostudies-arrayexpress

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2020-03-12 | E-MTAB-7679 | biostudies-arrayexpress

ASPSCR1-TFE3 reprograms transcription by organizing enhancers around hexameric VCP [hASPS_ChIP, histone_markers]

Project description:ChIPseq experiments identify that ASPSCR1-TFE3 defines active enhancers across the genome and co-distributes with VCP/p97. RNAseq after knock-down of ASPSCR1-TFE3 or VCP, inhibition of VCP, or overexpression of each in alveolar soft part sarcoma cell lines demonstrates their co-dependence. HiChIP defines chromatin conformations that surround ASPSCR1-TFE3 targets and are lost on VCP knock-down.

2023-01-01 | GSE162479 | GEO

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