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Genome-wide map of TRIM33, CDK9 and S2 Pol II binding sites in common dendritic cell progenitors

ABSTRACT: Transcriptional control of dendritic cell (DC) development has not been fully understood. TRIM33, a transcription co-factor was found to be crucial for transcription regulation during the development of DCs. Genome wide binding site analysis with CUT&Tag revealed co-localization of TRIM33 with CDK9 and Serine 2 phosphorylated RNA polymerase (S2 Pol II) in the common dendritic cell progenitors (CDPs).

ORGANISM(S): Mus musculus

PROVIDER: GSE255136 | GEO | 2024/06/01

REPOSITORIES: GEO

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Genome-wide map of TRIM33, CDK9 and S2 Pol II binding sites in common dendritic cell progenitors

Project description:Genome-wide map of TRIM33, CDK9 and S2 Pol II binding sites in common dendritic cell progenitors

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Genomewide mapping of Trim33 binding in Th17 cells

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.

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Dynamics of TRIM33 binding in macrophages and effects of TRIM33 deletion on chromatin state during activation of primary macrophages.

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).

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Compensatory induction of MYC expression by sustained CDK9 inhibition via a BRD4-dependent mechanism: Pol II occupancy profiling by ChIP-Seq in HeLa cell line in the presence or absence of CDK9 inhibition

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Genome-wide screening identifies Trim33 as an essential regulator of dendritic cell differentiation [Trim33 RNA-Seq]

Project description:The development of all dendritic cells (DCs) including antigen-presenting conventional DCs (cDCs) and cytokine-producing plasmacytoid DCs (pDCs) is controlled by the growth factor Flt3 ligand (Flt3L) and its receptor Flt3. We genetically dissected this common Flt3L-driven pathway of DCs differentiation using CRISPR/Cas9-based dropout screening in a Flt3L dependent progenitor cell line. Genome-wide screening identified multiple regulators of DC differentiation including the glycosylphosphatidylinositol transamidase complex and arginine methyltransferase Carm1, whose role was confirmed in vivo. It also showed that negative regulators of mTOR signaling, including the subunits of TSC and GATOR1 complexes, restricted progenitor growth but enabled DC differentiation, demonstrating that a TSC- and GATOR1-mediated shutdown of mTOR is required for the process. An orthogonal screen focused on transcriptional regulators showed that Trim33 (TIF-1g) is required for DC differentiation. Conditional targeting in vivo revealed an essential role of Trim33 in the development of all DCs, but not of monocytes or granulocytes. In particular, inducible deletion of Trim33 caused a rapid loss of all DC progenitors, pDCs and the cross-presenting cDC1 subset. The loss of Trim33 from DC progenitors caused spontaneous interferon and inflammatory response, aberrant induction of macrophage-specific genes, and failure to induce DC differentiation program. Collectively, these data elucidate common mechanisms that control Flt3L-driven differentiation of the entire DC lineage, and identify Trim33 as its essential regulator.

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The transcriptional cofactor TRIM33 prevents apoptosis in B lymphoblastic leukemia by deactivating a single enhancer [ChIP-Seq]

Project description:Most mammalian transcription factors and cofactors occupy thousands of genomic sites and modulate the expression of large gene networks to implement their biological functions. In this study, we describe an exception to this paradigm. TRIM33 is identified here as a lineage dependency in B cell neoplasms and is shown to perform this essential function by associating with a single cis element. ChIP-seq analysis of TRIM33 in murine B cell leukemia revealed a preferential association with two lineage-specific enhancers that harbor an exceptional density of motifs recognized by the PU.1 transcription factor. TRIM33 is recruited to these elements by PU.1, yet acts to antagonize PU.1 function. One of the PU.1/TRIM33 co-occupied enhancers is upstream of the pro-apoptotic gene Bim, and deleting this enhancer renders TRIM33 dispensable for leukemia cell survival. These findings reveal an essential role for TRIM33 in preventing apoptosis in B lymphoblastic leukemia by interfering with enhancer-mediated Bim activation. ChIP-Seq for Trim33, Pu.1 and histone modification marks in different types of leukemia cells

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