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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 [ChIP-seq]

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

PROVIDER: PRJNA480007 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11211668_1.fastq.gz	Fastqsanger.gz
	SRR11211668_2.fastq.gz	Fastqsanger.gz
	SRR11211669_1.fastq.gz	Fastqsanger.gz
	SRR11211669_2.fastq.gz	Fastqsanger.gz
	SRR11211670_1.fastq.gz	Fastqsanger.gz

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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.

Project description:Initial host response to mycobacterial infection is orchestrated through H3K4 methylation-mediated RNA polymerase II binding at key immune function genes.

| PRJNA480006 | ENA

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

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

| PRJNA480009 | ENA

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

| PRJNA480008 | ENA

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

2019-07-05 | GSE116732 | GEO

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

2019-07-05 | GSE116731 | GEO

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

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.

Project description:This SuperSeries is composed of the SubSeries listed below.

2019-07-05 | GSE116734 | GEO

Molecular insights into RNA polymerase recycling by mycobacterial HelD

Project description:Mycobacterial HelD is a transcription factor that binds RNA polymerase (RNAP) and thereby rescues it from stalled transcription complexes. HelD also protects RNAP against the antibiotic rifampicin. HelD, however, must be released from the rescued RNAP to participate in the next round of the transcription cycle. The exact mechanism of this release is unknown. Here we show that HelD from Mycobacterium smegmatis can form a complex with RNAP, together with σA primary sigma factor, and RbpA, but not CarD, transcription factors. Using cryo-EM, we solved a series of RNAP-σA-RbpA-HelD structures with or without promoter DNA. These snapshots capture the involvement of HelD in transcription initiation, describes mechanistic aspects of HelD release, and its protective effect against rifampicin. Biochemical evidence supports these findings, defines the role of ATP binding/hydrolysis to/by HelD in the process, and functionally confirms the rifampicin-protective effect of HelD. Taken together, HelD assists an alternative pathway of transcription initiation.

2024-10-08 | PXD046632 | Pride

Set1 H3K4 methyltransferase and Jhd2 H3K4 demethylase

Project description:Set1 H3K4 methyltransferase and Jhd2 H3K4 demethylase

| PRJNA296896 | ENA

Gene expression and cytokine profile correlate with mycobacterial growth in a human BCG challenge model

Project description:Bacille Calmette Guerin (BCG) is the most widely administered vaccine in the world yet its mechanism of action remains unclear. In this study, we have used samples from a human mycobacterial challenge study in which previously BCG-vaccinated or BCG-naïve UK adults were challenged intradermally with a standard dose of BCG vaccine. BCG remaining at the site of vaccination was quantified by polymerase chain reaction from a skin biopsy sample taken two weeks post-challenge and was used as a measure of BCG growth and functional anti-mycobacterial immunity. Using gene expression microarrays and flow cytometric analysis of intracellular cytokine production, we show that the magnitude of the immune response is greater in previously vaccinated volunteers and that this correlates with reduced mycobacterial growth but increased scarring at the vaccination site. In particular the IFNγ and IL-17 pathways are strongly induced in previously vaccinated volunteers and correlate with reduced mycobacterial growth in this population. This study supports the use of BCG challenge as a tool for evaluating vaccine efficacy and identifying mechanisms of anti-mycobacterial immunity

2014-12-01 | GSE58636 | GEO

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