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Batf pioneers the reorganization of chromatin in developing effector T cells via Ets1-dependent recruitment of Ctcf [ChIP-seq]

ABSTRACT: We have examined mechanisms by which Batf acts to initiate gene transcription in developing effector CD4 T cells. We find that in addition to its pioneering function, Batf controls developmentally regulated recruitment of the chromatin architectural factor, Ctcf, to promote chromatin looping that is associated with transcription of lineage-specific genes. The chromatin organizing actions of Batf are largely Ets1-dependent, which appears to be indispensable for the Batf-dependent recruitment of Ctcf. Moreover, most of the Batf-dependent sites to which Ctcf is recruited lie outside of Ap-1–Irf composite elements (AICEs), indicating that direct involvement of Batf-Irf complexes is not required. Thus, we have identified a cooperative role for Batf, Ets1 and Ctcf in chromatin reorganization that underpins transcriptional programming of effector T cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE123198 | GEO | 2019/11/04

REPOSITORIES: GEO

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Batf pioneers the reorganization of chromatin in developing effector T cells via Ets1-dependent recruitment of Ctcf [Hi-C]

Project description:We have examined mechanisms by which Batf acts to initiate gene transcription in developing effector CD4 T cells. We find that in addition to its pioneering function, Batf controls developmentally regulated recruitment of the chromatin architectural factor, Ctcf, to promote chromatin looping that is associated with transcription of lineage-specific genes. The chromatin organizing actions of Batf are largely Ets1-dependent, which appears to be indispensable for the Batf-dependent recruitment of Ctcf. Moreover, most of the Batf-dependent sites to which Ctcf is recruited lie outside of Ap-1–Irf composite elements (AICEs), indicating that direct involvement of Batf-Irf complexes is not required. Thus, we have identified a cooperative role for Batf, Ets1 and Ctcf in chromatin reorganization that underpins transcriptional programming of effector T cells.

2019-11-04 | GSE123208 | GEO

Batf pioneers the reorganization of chromatin in developing effector T cells via Ets1-dependent recruitment of Ctcf [ATAC-seq]

2019-11-04 | GSE123206 | GEO

Batf pioneers the reorganization of chromatin in developing effector T cells via Ets1-dependent recruitment of Ctcf

Project description:Batf pioneers the reorganization of chromatin in developing effector T cells via Ets1-dependent recruitment of Ctcf

| PRJNA507805 | ENA

Batf pioneers the reorganization of chromatin in developing effector T cells via Ets1-dependent recruitment of Ctcf [Hi-C]

Project description:Batf pioneers the reorganization of chromatin in developing effector T cells via Ets1-dependent recruitment of Ctcf [Hi-C]

| PRJNA507809 | ENA

Batf pioneers the reorganization of chromatin in developing effector T cells via Ets1-dependent recruitment of Ctcf [ChIP-seq]

Project description:Batf pioneers the reorganization of chromatin in developing effector T cells via Ets1-dependent recruitment of Ctcf [ChIP-seq]

| PRJNA507798 | ENA

Batf pioneers the reorganization of chromatin in developing effector T cells via Ets1-dependent recruitment of Ctcf [ATAC-seq]

Project description:Batf pioneers the reorganization of chromatin in developing effector T cells via Ets1-dependent recruitment of Ctcf [ATAC-seq]

| PRJNA507804 | ENA

BATF-JUN is critical for IRF4-mediated transcription in T cells

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. Genome-wide transcription factors mapping and binding of IRF4, BATF, IRF8, STAT3, JUN etc in WT, Irf4-/- and Batf-/- mice in different cell types (B cells, CD4+ T cells and TH17 cells) cultured with or without IL-21 was conducted. RNA-Seq is conducted in mouse B cells, CD4+ T cells, TH1/TH2/TH9/TH17/Treg.

2012-09-18 | E-GEOD-39756 | biostudies-arrayexpress

BATF-JUN is critical for IRF4-mediated transcription in T cells

2012-09-18 | GSE39756 | GEO

Epigenomics of Human CD8 T cell Differentiation and Aging

Project description:<p>The efficacy of the adaptive immune response declines dramatically with age, but the cell-intrinsic mechanisms driving the changes characteristic of immune aging in humans remain poorly understood. One hallmark of immune aging is the loss of self-renewing naive cells and the accumulation of differentiated but dysfunctional cells within the CD8 T cell compartment. Using ATAC-seq, we first inferred the transcription factor binding activities that maintain the naive and central and effector memory CD8 T cell states in young adults. Integrating our results with RNA-seq, we determined that BATF, ETS1, Eomes, and Sp1 govern transcription networks associated with specific CD8 T cell subset properties, including activation and proliferative potential. Extending our analysis to aged humans, we found that the differences between memory and naive CD8 T cells were largely preserved across age, but that naive and central memory cells from older individuals exhibited a shift toward a more differentiated pattern of chromatin openness. Additionally, aged naive cells displayed a loss in chromatin openness at gene promoters, a phenomenon that appears to be due largely to a loss in binding by NRF1, leading to a marked drop-off in the ability of the naive cell to initiate transcription of mitochondrial genes. Our findings identify BATF- and NRF1-driven gene regulation as targets for delaying CD8 T cell aging and restoring T cell function.</p>

| phs001187 | dbGaP

Comparison of gene expression profiles of naÃ¯ve and in vitro effector CD8+ T cells from wild-type and BATF-/- mice

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. P14 TCR transgenic CD8+ T cells from wild-type or BATF-/- mice were examined either as naÃ¯ve cells or after 3 days of in vitro stimulation with antibodies to CD3 and CD28 in the presence of IL-2

2014-03-02 | E-GEOD-54215 | biostudies-arrayexpress

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