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TBL1XR1 mutations bias germinal center B-cells towards a pro-tumorigenic memory fate

ABSTRACT: TBL1XR1 mutations bias germinal center B-cells towards a pro-tumorigenic memory fate

PROVIDER: PRJNA580268 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR10360845.fastq.gz	Fastqsanger.gz
	SRR10360846.fastq.gz	Fastqsanger.gz
	SRR10360847.fastq.gz	Fastqsanger.gz
	SRR10360848.fastq.gz	Fastqsanger.gz
	SRR10360849.fastq.gz	Fastqsanger.gz

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TBL1XR1 mutations bias germinal center B-cells towards a pro-tumorigenic memory fate

Project description:Diffuse large B-cell lymphomas (DLBCL) encompass a heterogeneous group of diseases derived from different stages of B-cell differentiation. The most clinically aggressive forms of DLBCL, C5/MCD, carry activating mutations in canonical B-cell signaling pathways, as well as early-occurring hits in the poorly-characterized gene TBL1XR1. Here, we investigated the role of TBL1XR1 mutations in the early steps of malignant transformation. We found that TBL1XR1 mutations disrupt germinal center development, and introduce a cell fate bias towards memory B (MB) cells. At the molecular level, TBL1XR1 mutations trigger a switch, by which the SMRT/HDAC3 co-repressor complex shuttles between the lineage-defining transcription factors BCL6 and BACH2. We further demonstrate that terminal differentiation of TBL1XR1 mutant MB is limited upon recall, and that these MB re-enter the germinal center reaction instead, suggesting a role for these cells as the cell-of-origin of C5/MCD DLBCL.

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Project description:Our spatiotemporal data confirmed activation of Tbl1xr1 in hepatocytes after 2/3 hepatectomy. TBL1XR1 is a transcriptional cofactor inducing ubiquitination and degradation of NCoR/SMRT co-repressors and NCoR is a negative regulator of hepatocyte proliferation acting through histone deacetylases (HDACs). We have examined the role of TBL1XR1 in liver regeneration through in vivo shRNA knockdown using adeno-associated viruses (shNC and shTbl1xr1) specifically targeting hepatocytes. The knockdown of Tbl1xr1 results in impair hepatocyte proliferation.To investigate the downstream targets of TBL1XR1 during liver regenration, we here perform the bulk RNA-seq for shNC and shTbl1xr1 at D2 after hepatectomy. Our data show demonstrated that Tbl1xr1 knockdown not only led to reduced cell cycle genes but also to impaired fatty acid β-oxidation as the most obviously affected liver function.

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Project description:Germinal center B cells were isolated from human tonsil tissue and crosslinked. ChIP was performed on two distinct pools of germinal center cells, each obtained from 3-5 donors. The experiment includes two biological replicates (germinal center cell pools from different donors). ChIP was performed on both pools and subject to library preparation and sequencing. Input DNA was sequenced for both pools.

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TBL1XR1 MUTATIONS DRIVE EXTRANODAL LYMPHOMA BY INDUCING A PRO-TUMORIGENIC MEMORY FATE

Project description:Data contains LC-MS data of proximity-based biotin labeling assay (BioID) to generate the protein interaction network of TBL1XR1 (WT and Y446S mutant) protein fused with to FlagBirA (N-terminal tag) and expressed in U2932 and OCILY1 cells.

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Gene Expression Profiles of Germinal Center B Cells

Project description:We report the gene expression profiles of germinal center B cells obtained by FACS analyses of normal human lymph nodes. We used FACS analyses to isolate germinal center B cells from 3 different individuals with one individual sampled twice. The overall goal was simply to identify genes that are highly expressed or silent in these purified cell populations.

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