ChIP-Seq of IRF4, BATF, and vIRF3 in BC-3 cells
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA548953 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR9304910.fastq.gz | Fastqsanger.gz | |||
| SRR9304911.fastq.gz | Fastqsanger.gz | |||
| SRR9304912.fastq.gz | Fastqsanger.gz | |||
| SRR9304903.fastq.gz | Fastqsanger.gz | |||
| SRR9304904.fastq.gz | Fastqsanger.gz |
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Project description:The Kaposi's sarcoma-associated herpesviruses causes several cancers including Kaposi's sarcoma and primary effusion lymphoma (PEL). Our work reveals that the cellular transcription factors interferon regulatory factor 4 (IRF4) and basic leucine zipper ATF-like transcription factor (BATF), as well as the viral interferon regulatory factor 3 (vIRF3) are critical oncogenic dependencies specific to PEL cell lines. To understand the functions of these transcription factors, we performed ChIP-Seq on these proteins in BC-3 PEL cell line. Our results reveal that these oncogenic factors may cooperate to regulate the expression of the same mRNAs.
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Project description:The Kaposi's sarcoma-associated herpesviruses causes several cancers including Kaposi's sarcoma and primary effusion lymphoma (PEL). Our work reveals that the cellular transcription factors interferon regulatory factor 4 (IRF4) and basic leucine zipper ATF-like transcription factor (BATF), as well as the viral interferon regulatory factor 3 (vIRF3) are critical oncogenic dependencies specific to PEL cell lines. To understand the functions of these transcription factors, we performed mRNA-Seq on the PEL BC-3 cell lines that have been targeted for CRISPR/Cas9 IRF4 KO, BATF KO and MDM4 KO (as unrelated negative control) and CRISPRi-mediated vIRF3 KD. Our results reveal that these oncogenic factors may cooperate to regulate the expression of the same mRNAs.
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Project description:The transcription factor BATF is required for Th17 and TFH differentiation. Here, we show that BATF also has a fundamental role in regulating effector CD8+ T cell differentiation. BATF-deficient CD8+ T cells show profound defects in effector expansion and undergo proliferative and metabolic catastrophe early after antigen encounter. BATF, together with IRF4 and Jun proteins, binds to and promotes early expression of genes encoding lineage-specific transcription-factors (T-bet and Blimp-1) and cytokine receptors, while paradoxically repressing genes encoding effector molecules (IFNg and granzyme B). Thus, BATF amplifies TCR-dependent transcription factor expression and augments inflammatory signal propagation but restrains effector gene expression. This checkpoint prevents irreversible commitment to an effector fate until a critical threshold of downstream transcriptional activity has been achieved. This is an examination of 5 different transcription factors (TFs) with 5 different histone modifications in effector CD8+ T cells. Two of the TFs (BATF and IRF4) and the histone modifications were replicated. Appropriate control sequence files for ChIP input, IgG ChIP, and Total H3 are also included.
2014-03-02 | E-GEOD-54191 | biostudies-arrayexpress
Project description:Purpose: The purpose of this study is to find the binding partner of IRF4 in the context of Th17- cell differentiation. To this end, we have used ChIPseq analysis followed by de novo motif search around genome-wide binding sites to identify BATF as the binding partner for IRF4 in the context of not only Th17 cells but other immune cell types as well. Naïve T-cells isolated from the spleen of C57BL/6J mice are cultured under Th17, Th2 or Th0 polarizing conditions for 42 hrs and subject to ChIP using IRF4 and/or BATF antibodies followed by high-throughput sequencing. Bone marrow derived dendritic cells (BMDCs) were stimulated with LPS for 6hrs and similrly subjected to ChIPseq analysis with IRF4.
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Project description:Variable strengths of signaling via the T cell antigen receptor (TCR) can produce divergent outcomes, but the mechanism of this remains obscure. The abundance of the transcription factor IRF4 increases with TCR signal strength, but how this would induce distinct types of responses is unclear. We compared the expression of genes in the TH2 subset of helper T cells to enhancer occupancy by the BATF–IRF4 transcription factor complex at varying strengths of TCR stimulation. Genes dependent on BATF–IRF4 clustered into groups with distinct TCR sensitivities. Enhancers exhibited a spectrum of occupancy by the BATF–IRF4 ternary complex that correlated with the sensitivity of gene expression to TCR signal strength. DNA sequences immediately flanking the previously defined AICE motif controlled the affinity of BATF–IRF4 for direct binding to DNA. Analysis by the chromatin immunoprecipitation–exonuclease (ChIP-exo) method allowed the identification of a previously unknown high-affinity AICE2 motif at a human single-nucleotide polymorphism (SNP) of the gene encoding the immunomodulatory receptor CTLA-4 that was associated with resistance to autoimmunity. Thus, the affinity of different enhancers for the BATF–IRF4 complex might underlie divergent signaling outcomes in response to various strengths of TCR signaling
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Project description:Interferon regulatory factor 4 (IRF4) is an IRF family transcription factor with critical roles in lymphoid development and in regulating the immune response. IRF4 binds DNA weakly owing to a carboxy-terminal auto-inhibitory domain, but cooperative binding with factors such as PU.1 or SPIB in B cells increases binding affinity, allowing IRF4 to regulate genes containing ETS–IRF composite elements (EICEs; 5'-GGAAnnGAAA-3'). Here we show that in mouse CD4+ T cells, where PU.1/SPIB expression is low, and in B cells, where PU.1 is well expressed, IRF4 unexpectedly can cooperate with activator protein-1 (AP1) complexes to bind to AP1–IRF4 composite (5'-TGAnTCA/GAAA-3') motifs that we denote as AP1–IRF composite elements (AICEs). Moreover, BATF–JUN family protein complexes cooperate with IRF4 in binding to AICEs in pre-activated CD4+ T cells stimulated with IL-21 and in TH17 differentiated cells. Importantly, BATF binding was diminished in Irf4-/- T cells and IRF4 binding was diminished in Batf-/- T cells, consistent with functional cooperation between these factors. Moreover, we show that AP1 and IRF complexes cooperatively promote transcription of the Il10 gene, which is expressed in TH17 cells and potently regulated by IL-21. These findings reveal that IRF4 can signal via complexes containing ETS or AP1 motifs depending on the cellular context, thus indicating new approaches for modulating IRF4-dependent transcription.
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