Genomewide mapping of Trim33 binding in Th17 cells
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ABSTRACT:
PROVIDER: PRJNA464365 | ENA |
REPOSITORIES: ENA
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Project description:We report the genome-wide binding of Trim33 in Th17 cells. We found that more than 90% of Trim33 binding regions was located in non-conding sequence, and therefore reflect the role of Trim33 as a trancriptional co-factor. Trim33 was found to accumulate on cis-regulatory regions of genes that regulate the function of Th17 cells such as Il17a, Ccr6 and Il10. This study provides a basis for the comprehensive understanding of Trim33-mediated regulation of Th17 cells.
2018-05-08 | GSE114119 | GEO
Project description:We report that Tripartite motif-containing 33 (Trim33), a protein that was previously associated with TGF-beta signaling, determines the pathogenic function of Th17 cells. Trim33 deficiency in T cells resulted in resistance to an autoimmune disease model. Lack of Trim33 did not impact TGF-beta signaling in mediating Foxp3 gene expression but greatly reduced TGF-beta induction of IL-17 production during Th17 cell differentiation. Importantly, we found TGF-beta not only increased IL-17 but also suppressed IL-10 expression; absence of Trim33 or Smad2 but not Smad4 in T cells enhanced IL-10 expression. In a Smad2-dependent manner, Trim33 was recruited to Il17 and Il10 gene loci and was crucial in appropriate histone modification accompanying Th17 differentiation. Our study thus demonstrates that Trim33, a non-canonical branch of TGF-beta signaling, programs the pro-inflammatory function of Th17 differentiation by promoting IL-17 and suppressing IL-10 expression. As a critical switch of pathogenic versus regulatory phenotype of T cells, Trim33 may be targeted in treating human autoimmune diseases.
2018-05-02 | GSE113925 | GEO
Project description:To get insight into TRIM33 functions, TRIM33 ChIP-seq was carried out in murine macrophage cell line (RAW) and in bone marrow-derived macrophages (BMDM). The results showed that, in addition to its role in hematopoietic differentiation, TRIM33 may modulate PU.1 transcriptional activity during macrophage development and/or activation.To characterize the role of TRIM33 in macrophages, we bred TRIM33fl/fl mice with Lyz-Cre mice where the Cre recombinase gene is under the regulatory sequences of the Lyz gene that is expressed only in mature myeloid cells. Bone marrow cells from LyzCre/Trim33+/+ mice and LyzCre/Trim33flox/flox mice were differentiated in macrophages and treated during 0h, 4h, 12h and 24h with LPS. Using ChIP-seq, we provide a link between TRIM33 binding and H3K4me3 spreading on inflammatory genes in macrophages. Chromatin immunoprecipitations of TRIM33 and H3K4Me3 followed by multiparallel sequencing performed in murine bone marrow-derived macrophages (BMDM).
2015-11-23 | E-GEOD-43654 | biostudies-arrayexpress
Project description:To get insight into TRIM33 functions, TRIM33 ChIP-seq was carried out in murine macrophage cell line (RAW) and in bone marrow-derived macrophages (BMDM). The results showed that, in addition to its role in hematopoietic differentiation, TRIM33 may modulate PU.1 transcriptional activity during macrophage development and/or activation.To characterize the role of TRIM33 in macrophages, we bred TRIM33fl/fl mice with Lyz-Cre mice where the Cre recombinase gene is under the regulatory sequences of the Lyz gene that is expressed only in mature myeloid cells. Bone marrow cells from LyzCre/Trim33+/+ mice and LyzCre/Trim33flox/flox mice were differentiated in macrophages and treated during 0h, 4h, 12h and 24h with LPS. Using ChIP-seq, we provide a link between TRIM33 binding and H3K4me3 spreading on inflammatory genes in macrophages.
2015-11-23 | GSE43654 | GEO
Project description:Genomewide identification of ANAC060 binding targets
| PRJNA507758 | ENA
Project description:We report high throughput profiling and co-occupancy of Trim33, Ctcf and H3K27ac in differentiating embryoid bodies derived from mouse embryonic stem cells. An average of ~37 million reads were generated for each of the described samples and input sample generating 4,426, 52,446, 30,047 peaks respectively for Trim33, CTCF and H3K27ac. Motif enrichment analyses for Trim33 ChiP-Seq data returned CTCF and BORIS (CTCF analog) motifs as best matches. Of the merged peaks, 723 were shared by Trim33, CTCF as well as H3K27ac. In addition, 1299 peaks were shared by Trim33 and CTCF, 1131 were shared by Trim33 and H3K27ac and 3321 were shared by CTCF and H3K27ac.
2019-01-01 | GSE119874 | GEO
Project description:To get insight into lineage-specific TRIM33 functions, TRIM33 ChIP-seq was carried out in non-differentiated erythroid (MEL NI), differentiated erythroid (MEL I), immature myeloid (32D). In addition, we compared the genome-wide profiles of RNA PolII occupancy between wild-type bone marrow-derived macrophages (BMDM) and Trim33-/- BMDM activated with LPS.
2021-09-17 | GSE73448 | GEO
Project description:Tripartite motif-containing 33 (Trim33) determines the pathogenic function of Th17 cells
| PRJNA454473 | ENA
Project description:The differentiation of Th17 cells is controlled by a complex network of transcription factors (TFs), including FOS and JUN proteins of the AP-1 family. The FOS-like proteins, FOSL1 and FOSL2 have recently been reported to control Th17 responses. The molecular mechanisms dictating their roles, however, are unclear. Moreover, although the functions of AP-1 TFs are largely governed by their protein-protein interactions, these are also poorly characterized in this milieu. Using affinity purification in combination with mass-spectrometry we established the first interactomes of FOSL1 and FOSL2 in human Th17 cells. In addition to their known interactions with JUN proteins, our analysis identified several novel binding partners of FOSL factors. Gene ontology analysis revealed RNA binding was enriched as the major functionality for FOSL1 and FOSL2 associated proteins, thereby suggesting possible mechanistic links that have not been studied before. Intriguingly, 29 interactors were found to be shared between FOSL1 and FOSL2, which included crucial regulators of Th17-fate. These findings, including unique and shared interactions, were validated using parallel reaction monitoring targeted mass-spectrometry (PRM-MS), with additional measurements with other laboratory methods. Overall, this study provides key insights into interaction-based signalling mechanisms of FOSL1 and FOSL2, which potentially control Th17 cell-development and associated pathologies.
2021-11-02 | PXD025729 | Pride
Project description:Transposable elements (TEs) have been active in the mammalian genome for hundreds of millions of years and each TE has had a distinct period of transpositional activity, followed by inactivation. Mice carrying reporter transgenes can be used to model transcriptional silencing at TEs. A mutagenesis screen for modifiers of epigenetic gene silencing produced a line with a null mutation in Trim33. Heterozygous mutants displayed increased expression of the reporter transgene. ChIP-seq of Trim33 in testis revealed 9,109 peaks, mostly at promoters, across the mouse genome. Trim33 was enriched at many RLTR10B elements that are among the youngest retrotransposons in the mouse genome. RNA-seq revealed that testis of mice haploinsufficient for Trim33 had altered expression of a small group of genes. The gene with the most significant increase, Nmnat3, was found to be transcribed from an upstream RLTR10B element. We show that Trim33 is involved in repressing RLTR10B elements in mouse testis. Examination of Trim33 binding using ChIP sequencing and the result of Trim33 haploinsufficiency using RNA sequencing, in mouse testis
2015-11-06 | E-GEOD-68617 | biostudies-arrayexpress