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

ABSTRACT: 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

ORGANISM(S): Homo sapiens

PROVIDER: GSE86811 | GEO | 2016/10/11

SECONDARY ACCESSION(S): PRJNA342602

REPOSITORIES: GEO

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

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 transcriptome.

2016-10-11 | GSE86813 | GEO

Assessing the impact of loss of MORC2 and SETDB1 on the global distribution of H3K9me3

Project description:By comparing HeLa cells lacking MORC2 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 MORC2 on the distribution of the repressive H3K9me3 histone modification.

2017-05-29 | GSE95456 | GEO

Targeting the Atf7ip-Setdb1 complex augments anti-tumor immunity by boosting tumor immunogenicity

Project description:Despite substantial progress that has been made in understanding how tumors escape immune surveillance, measures to counteract tumor immune evasion have been limited. Suppression of tumor antigen expression is a common adaptive mechanism that cancers use to evade detection and destruction by the immune system. Epigenetic modifications play a critical role in in various aspects of immune invasion, including the regulation of tumor antigen expression. To identify novel epigenetic regulators of tumor antigen expression, we established a transplantable syngeneic tumor model of immune escape with silenced antigen expression and used this system as a platform for a CRISPR-Cas9 suppressor screen targeting genes encoding epigenetic modifiers. We found that genetic disruption of the chromatin modifiers Atf7ip or its interacting partner Setdb1 in tumor cells restored tumor antigen expression, resulting in augmented tumor immunogenicity concomitant with elevated endogenous retroviral antigens (ERVs), mRNA intron retention. ERVs disinhibition was associated with a robust type I interferon response and increased T cell infiltration, leading to rejection of cells lacking intact Atf7ip or Setdb1. ATF7IP or SETDB1 expression inversely correlated with antigen processing and presentation pathways, interferon signaling, and T cell infiltration and cytotoxicity in human cancers. Our results provide a rationale for targeting Atf7ip or Setdb1 in cancer immunotherapy.

2021-07-23 | GSE179574 | GEO

H3K9me3 ChIP-seq in HeLa cells lacking TASOR, MPP8, periphilin and SETDB1

Project description:We performed ChIP-seq to measure H3K9me3 levels in wild-type HeLa cells and HeLa cells lacking TASOR, MPP8, periphilin and SETDB1 generated through CRISPR/Cas9-mediated gene disruption.

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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.

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SETDB1 suppresses interferon responses and NK cell-mediated immunosurveillance specifically in monocytic AML: H3K9me3 ChIP-seq of cSAM leukemia cells with Setdb1 depletion [ChIP-seq]

Project description:Monocytic acute myeloid leukemia (AML) responds poorly to current treatments, including venetoclax-based therapy. We conducted in vivo and in vitro CRISPR/Cas9 library screenings using a mouse monocytic AML model, and identified SETDB1 and its binding partners (ATF7IP and TRIM33) as crucial tumor promoters in vivo. The growth-inhibitory effect of Setdb1 depletion in vivo was mainly dependent on NK cell-mediated cytotoxicity. Mechanistically, SETDB1 depletion upregulated interferon-stimulated genes and NKG2D ligands through demethylation of histone H3 Lys9 at the monocyte-specific enhancer regions, thereby enhancing their immunogenicity to NK cells and intrinsic apoptosis. Importantly, these effects were not observed in non-monocytic leukemia cells. We also identified the expression of MNDA and its murine counterpart Ifi203 as biomarkers to predict the sensitivity of each AML to SETDB1 depletion. Our study highlights the critical and selective role of SETDB1 in monocytic AML and underscores its potential as a therapeutic target for current unmet needs.

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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

Targeting the Atf7ip-Setdb1 complex augments anti-tumor immunity by boosting tumor immunogenicity

Project description:Targeting the Atf7ip-Setdb1 complex augments anti-tumor immunity by boosting tumor immunogenicity

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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.

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SETDB1 suppresses interferon responses and NK cell-mediated immunosurveillance specifically in monocytic AML: Gene expression profiles of cSAM leukemia cells with Setdb1 depletion [RNA-seq]

2024-08-03 | GSE266097 | GEO