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ATF7ip targets transposable elements for H3K9me3 deposition to modify CD8+ T cell effector and memory responses [ChIP-seq]

ABSTRACT: ATF7ip targets transposable elements for H3K9me3 deposition to modify CD8+ T cell effector and memory responses [ChIP-seq]

PROVIDER: PRJNA787789 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17194430.fastq.gz	Fastqsanger.gz
	SRR17194432.fastq.gz	Fastqsanger.gz
	SRR17194433.fastq.gz	Fastqsanger.gz
	SRR17194434.fastq.gz	Fastqsanger.gz
	SRR17194435.fastq.gz	Fastqsanger.gz

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ATF7ip targets transposable elements for H3K9me3 deposition to modify CD8+ T cell effector and memory responses [ChIP-seq]

Project description:CD8+ T cells are critical for the adaptive immune response to infection and tumors. Moreover, CD8+ T cell memory is important for the immune systems response to repeat infections. Here, we identify the activating transcription factor 7 interacting protein as a critical regulator of CD8+ T cell memory and effector responses. Mice with a T cell specific deletion of ATF7ip have a CD8+ T cell intrinsic enhancement of Il7r expression and Il2 expression leading to enhanced memory responses. ChIP-seq studies identified ATF7ip as an inhibitor of Il7r and Il2 gene expression through the deposition of the repressive histone mark H3K9me3 in the Il7r gene loci and Il2-Il21 intergenic region. Interestingly, ATF7ip targeted transposable elements (TE) for H3K9me3 in these regions. These results demonstrate a new epigenetic pathway by which IL7r and IL-2 production are constrained in CD8+ T cells, and this may open up new avenues for modulating their production.

2021-12-21 | GSE190624 | GEO

ATF7ip targets transposable elements for H3K9me3 deposition to modify CD8+ T cell effector and memory responses

Project description:ATF7ip targets transposable elements for H3K9me3 deposition to modify CD8+ T cell effector and memory responses

| PRJNA787083 | ENA

ATF7ip targets transposable elements for H3K9me3 deposition to modify CD8+ T cell effector and memory responses

Project description:Method: To study the effector response of Atf7ip, a) we infected Atf7ip+/fl and Atf7ipfl/fl mice with lcmv . RNAseq was performed using CD8 T cells isolated from Lymph node and Spleen of Het and KO mice. RNA was isolated using Qiagen RNeasy Mini Kit as per manufacturers protocol. The RNA-Seq was performed by UCSF core using Illumina Platform. RNAseq was also carried out using naive CD8 T cells isolated from Atf7ip+/fl and Atf7ipfl/fl mice along with Atf7ip+/fl and Atf7ipfl/fl CD8 T cells stimulated for 72 hrs. This set of samples were sequenced using commercial facility from Genewiz, USA. Results: Our transcriptome analysis (RNA-seq) identified, Il7r, Runx3 etc. to be upregulated in the Atf7ipfl/fl CD8 T cells as compared to the Atf7ip+/fl CD8 T cells.

2021-12-21 | GSE190417 | GEO

H3K9me3 ChIP-seq in ATF7ip Knockout naïve T cells

Project description:T helper 17 cells (Th17) are critical for fighting infections at mucosal surfaces, however, they have also been found to contribute to the pathogenesis of multiple autoimmune diseases and Th17 cells have been targeted therapeutically. Due to the role of Th17 cells in autoimmune pathogenesis, it is important to understand the factors that control Th17 development. Here we identify the activating transcription factor 7 interacting protein (ATF7ip) as a critical regulator of Th17 differentiation. Mice with T-cell-specific deletion of Atf7ip have impaired Th17 differentiation secondary to the aberrant overproduction of IL-2 with T-cell receptor (TCR) stimulation and are resistant to colitis in vivo. ChIP-seq studies identified ATF7ip as an inhibitor of Il2 gene expression through the deposition of the repressive histone mark H3K9me3 in the Il2-Il21 intergenic region. These results demonstrate a new epigenetic pathway by which IL-2 production is constrained and this may open up new avenues for modulating its production.

2019-05-21 | GSE131511 | GEO

H3K9me3 ChIP-seq in ATF7ip Knockout naïve T cells

Project description:H3K9me3 ChIP-seq in ATF7ip Knockout naïve T cells

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RNA-seq of ATF7ip-deficient T cells

Project description:RNA-seq performed in ATF7ip-deficient T cells reveals a defect in Th17 gene induction secondary to increased IL-2 T helper 17 cells (Th17) are critical for fighting infections at mucosal surfaces, however, they have also been found to contribute to the pathogenesis of multiple autoimmune diseases and Th17 cells have been targeted therapeutically. Due to the role of Th17 cells in autoimmune pathogenesis, it is important to understand the factors that control Th17 development. Here we identify the activating transcription factor 7 interacting protein (ATF7ip) as a critical regulator of Th17 differentiation. Mice with T-cell-specific deletion of Atf7ip have impaired Th17 differentiation secondary to the aberrant overproduction of IL-2 with T-cell receptor (TCR) stimulation and are resistant to colitis in vivo. ChIP-seq studies identified ATF7ip as an inhibitor of Il2 gene expression through the deposition of the repressive histone mark H3K9me3 in the Il2-Il21 intergenic region. These results demonstrate a new epigenetic pathway by which IL-2 production is constrained and this may open up new avenues for modulating its production.

2019-05-21 | GSE131533 | GEO

Assessing the impact of loss of ATF7IP and SETDB1 on the global distribution of H3K9me3

Project description:By comparing HeLa cells lacking ATF7IP or SETDB1 generated through CRISPR/Cas9-mediated gene disruption to wild-type HeLa cells, the goal of the experiment was to determine the effect of loss of the SETDB1•ATF7IP complex on the distribution of the repress

2016-10-11 | GSE86811 | GEO

Paramecium Polycomb Repressive Complex 2 physically interacts with the small RNA binding PIWI protein to repress transposable elements

Project description:Polycomb Repressive Complex 2 (PRC2) maintains transcriptionally silent genes in a repressed state via deposition of histone H3 K27 trimethyl (me3) marks. PRC2 has also been implicated in silencing transposable elements (TEs) yet how PRC2 is targeted to TEs remains unclear. To address this question, we performed tandem affinity purification combined with mass spectrometry and identified proteins that physically interact with the Paramecium Enhancer-of-zeste Ezl1 enzyme, which catalyzes H3K9me3 and H3K27me3 deposition at TEs. We show that the Paramecium PRC2 core complex comprises four subunits, each required in vivo for catalytic activity. We also identify PRC2 cofactors, including the RNA interference (RNAi) effector Ptiwi09, which are necessary to target H3K9me3 and H3K27me3 to TEs. We find that the physical interaction between PRC2 and the RNAi pathway is mediated by a RING finger protein and that small RNA recruitment of PRC2 to TEs is analogous to the small RNA recruitment of H3K9 methylation SU(VAR)3-9 enzymes.

2022-04-06 | PXD031335 | Pride

TNRC18 recognizes H3K9me3 to mediate transposable elements silencing at ERV regions

Project description:TNRC18 recognizes H3K9me3 to mediate transposable elements silencing at ERV regions

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Assessing the impact of loss of ATF7IP and SETDB1 on the transcriptome

2016-10-11 | GSE86813 | GEO