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Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation.

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Homo sapiens

PROVIDER: GSE116698 | GEO | 2019/10/16

REPOSITORIES: GEO

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AP-1 activity induced by co-stimulation is required for chromatin opening during T cell activation.

Project description:Activation of T cells is dependent on the organized and timely opening and closing of chromatin. Herein, we identify AP-1 as the transcription factor that directs most of this remodeling. Chromatin accessibility profiling showed quick opening of closed chromatin in naive T cells within 5 h of activation. These newly opened regions were strongly enriched for the AP-1 motif, and indeed, ChIP-seq demonstrated AP-1 binding at >70% of them. Broad inhibition of AP-1 activity prevented chromatin opening at AP-1 sites and reduced the expression of nearby genes. Similarly, induction of anergy in the absence of co-stimulation during activation was associated with reduced induction of AP-1 and a failure of proper chromatin remodeling. The translational relevance of these findings was highlighted by the substantial overlap of AP-1-dependent elements with risk loci for multiple immune diseases, including multiple sclerosis, inflammatory bowel disease, and allergic disease. Our findings define AP-1 as the key link between T cell activation and chromatin remodeling.

| S-EPMC7037242 | biostudies-literature

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ChIP-seq]

Project description:Activation of T cells is dependent on organized and timely opening and closing of chromatin. We perform ATAC-seq (subseries 1), ChIP-seq (subseries 2), and RNA-seq (subseries 3) at 5, 24, and 60 h of T cell activation with anti-CD3 and -CD28 antibodies in human primary naïve CD4 T cells. We report that chromatin opening at early time points is established by AP-1 transcription factor and associated with transcriptional enhancer identified as risk loci for multiple immune diseases in human naïve CD4 T cells.

2019-10-16 | GSE116695 | GEO

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [RNA-seq]

2019-10-16 | GSE116697 | GEO

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ATAC-seq]

2019-10-16 | GSE116696 | GEO

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation.

Project description:Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation.

| PRJNA479881 | ENA

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ChIP-seq]

Project description:Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ChIP-seq]

| PRJNA479884 | ENA

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ATAC-seq]

Project description:Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [ATAC-seq]

| PRJNA479883 | ENA

Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [RNA-seq]

Project description:Co-Stimulation–Induced AP-1 Activity is Required for Chromatin Opening During T Cell Activation [RNA-seq]

| PRJNA479885 | ENA

The Breakdown of Stored Triacylglycerols Is Required during Light-Induced Stomatal Opening.

Project description:Stomata regulate the uptake of CO2 and the loss of water vapor [1] and contribute to the control of water-use efficiency [2] in plants. Although the guard-cell-signaling pathway coupling blue light perception to ion channel activity is relatively well understood [3], we know less about the sources of ATP required to drive K(+) uptake [3-6]. Here, we show that triacylglycerols (TAGs), present in Arabidopsis guard cells as lipid droplets (LDs), are involved in light-induced stomatal opening. Illumination induces reductions in LD abundance, and this involves the PHOT1 and PHOT2 blue light receptors [3]. Light also induces decreases in specific TAG molecular species. We hypothesized that TAG-derived fatty acids are metabolized by peroxisomal β-oxidation to produce ATP required for stomatal opening. In silico analysis revealed that guard cells express all the genes required for β-oxidation, and we showed that light-induced stomatal opening is delayed in three TAG catabolism mutants (sdp1, pxa1, and cgi-58) and in stomata treated with a TAG breakdown inhibitor. We reasoned that, if ATP supply was delaying light-induced stomatal opening, then the activity of the plasma membrane H(+)-ATPase should be reduced at this time. Monitoring changes in apoplastic pH in the mutants showed that this was the case. Together, our results reveal a new role for TAGs in vegetative tissue and show that PHOT1 and PHOT2 are involved in reductions in LD abundance. Reductions in LD abundance in guard cells of the lycophyte Selaginella suggest that TAG breakdown may represent an evolutionarily conserved mechanism in light-induced stomatal opening.

| S-EPMC4791430 | biostudies-literature

TCR stimulation upregulates MS4a4B expression through induction of AP-1 transcription factor during T cell activation.

Project description:MS4a4B is a novel member of the membrane-spanning 4-domain family, subfamily A (MS4A) specifically expressed in mouse T cells. We have shown previously that expression of MS4a4B in T cells is upregulated upon T cell activation, suggesting that MS4a4B may play a functional role in regulation of T cell responses. However, little is known about the mechanisms that regulate MS4a4B gene expression. In this study, we explored the potential mechanism underlying TCR-stimulation-induced expression of MS4a4B by promoter analysis. We cloned 2495bp of 5'-flanking region upstream of the MS4a4B start code and inserted the DNA fragment into pGL4.20 reporter plasmid. To analyze promoter activity of the cloned DNA fragment, we transiently transfected EL4 thymoma cells and the T32 cell line with reporter plasmids. Expression of reporter gene was determined by dual-luciferase assay. Potential activator- and repressor-binding sites were analyzed by serial length of 5'-deletion. We have identified at least two potential activator binding regions and two potential repressor binding regions. The activator binding sites have been localized to two fragments, which are a 442-base pair region (region A) positioned from -1176 to -735, and a 119-base pair region (region B) positioned -188 to -70 respectively. MatInspector analysis showed that region A contains the consensus binding motif of the AP-1 family of transcription factors. Machinery analysis showed that nuclear proteins extracted from anti-CD3/anti-CD28-activated primary T cells specifically bind to the AP-1 binding element. In contrast, blockade by AP-1 inhibitor in culture decreased MS4a4B expression in T cells. Our data demonstrate that TCR-stimulation induces transactivation of AP-1 transcription factor, which subsequently binds to the MS4a4B promoter and upregulates expression of MS4a4B in activated T cells.

| S-EPMC4516228 | biostudies-literature

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