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The influence of the transcription factor EB for BCR-induced gene expression in murine WEHI-231 B cells

ABSTRACT: To investigate TFEB-dependent expression in BCR-stimulated and resting B cells, CRISPR/Cas9 knockout cell lines were established and subjected to RNA sequencing analysis

ORGANISM(S): Mus musculus

PROVIDER: GSE212457 | GEO | 2024/06/25

REPOSITORIES: GEO

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The influence of the transcription factor EB for BCR-induced gene expression in human Ramos B cells

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Transcription factor EB sets the stage for fate decisions of antigen-primed B cells in the absence and presence of co-stimulation

Project description:Ligation of the B cell antigen receptor (BCR) initiates humoral immunity. However, mere BCR signaling without appropriate co-stimulation commits B cells to death rather than to differentiation into immune effector cells. How BCR activation depletes potentially autoreactive B cells while simultaneously primes for receiving rescue and differentiation signals from cognate T lymphocytes remains unknown. Here, using a mass spectrometry-based proteomic approach to identify cytosolic/nuclear shuttling elements, we uncover transcription factor EB (TFEB) as a central BCR-controlled rheostat that drives activation-induced apoptosis, and concurrently, promotes the reception of co-stimulatory rescue signals by supporting B cell migration and antigen presentation. CD40 co-stimulation prevents TFEB-driven cell death, while enhancing and prolonging TFEB’s nuclear residency, which hallmarks antigenic experience also of memory B cells. In mice, TFEB shapes the transcriptional landscape of germinal center B cells. Within the germinal center, TFEB facilitates the dark zone entry of light-zone-residing centrocytes through regulation of chemokine receptors and, by balancing the expression of Bcl-2/BH3-only family members, integrates antigen-induced apoptosis with T cell-provided CD40 survival signals. Thus, TFEB reprograms antigen-primed germinal center B cells for cell fate decisions.

2024-08-08 | PXD054505 | Pride

Loss of transcription factor EB action remodel lipid metabolism and cell death pathways in the cardiomyocyte

Project description:Loss of TFEB action, impaired lysosomal autophagy and increased proteotoxicity are observed in numerous metabolic diseases. Previous research from our laboratory demonstrated that glucolipotoxicity following nutrient-overload causes cardiomyocyte injury by inhibiting TFEB and suppressing lysosomal function. However, the identity of signalling and metabolic pathways engaged by the loss of TFEB action in the cardiomyocytes remain unknown. In cardiomyocytes subjected to nutrient-overload ex-vivo, saturated fatty acid, palmitate, but not polyunsaturated fatty acids decreased TFEB content in a concentration- and time-dependent manner. Hearts from high-fat high-sucrose diet-fed mice also exhibited a temporal decline in nuclear TFEB content with marked elevation of distinct lipid species suggesting that when myocyte threshold of lipid loading exceeds its metabolic capacity, loss of TFEB and cardiomyocyte stress is observed. Transcriptome analysis in murine cardiomyocytes with targeted deletion of myocyte TFEB (TFEB-/-) revealed enrichment of differentially expressed genes (DEG) representing pathways of nutrient metabolism, DNA damage and repair, cell death and cardiac function. Strikingly, genes involved in autophagy, proteolysis and lysosome function constituted a small portion of DEGs in TFEB-/- cardiomyocytes signifying that TFEB plausibly regulates non-canonical pathways of cardiac energy metabolism than the canonical pathway of autophagy. TFEB-/- myocytes exhibited higher lipid droplet accumulation and increased caspase-3 activation. Under nutrient-overload condition, restoration of constitutive localization of TFEB in the myocyte nucleus abrogated increased lipid deposition and caspase-3 activity. Together, our data demonstrated that TFEB insufficiency and its loss of action in the cardiomyocyte remodels energy metabolism and renders the heart prematurely susceptible to nutrient overload-induced injury and failure.

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CEA_SGF:E00010#bcr-abl

Project description:Chronic myelogenous leukemia (CML) is a malignant disease of the hematopoietic stem cell, characterized by the expression of the Bcr-Abl oncogene by leukemic cells. In order to analyze the molecular pathways modulated by Bcr-Abl, we have previously generated an inducible model of Bcr-Abl expression in the murine Ba/F3 cell line based on the Tet-OFF system. In the present study, through a microarray approach applied to cells grown with (Bcr-Abl-expression OFF) or without (Bcr-Abl-expression ON) doxycycline, a tetracycline analogue, we analyzed the gene expression variations upon Bcr-Abl expression. Keywords: repeat sample

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Gene expression profiling of murine BCR-ABL+ CDK6-wt and CDK6-KO cells

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Expression data from murine hematopoietic cells expressing BCR-ABL alone, NUP98-HOXA9 alone, BCR-ABL and NUP98-HOXA9, or null for both oncogenes

Project description:Leukemia is a complex malignancy with hundreds of distinct mutations associated with disease development. Studies have shown that oncogenes cooperate to promote leukemia transformation, however, the downstream effectors of this cooperation are largely unknown. Using a genetically defined mouse model of acute leuekmia, we investigated the regulated of genes downstream of the cooperative oncogenic interaction between BCR-ABL and NUP98-HOXA9 and identified a unique gene signature abberrantly expression in leukemia. Total RNA was isolated from hematopoietic cells transduced with BCR-ABL and Nup98-HOXA9 retroviruses and transplanted into recipient mice. Bone marrow cells were purified by GFP (BCR-ABL) and YFP (NUP98-HOXA9) using FACS.

2012-05-10 | E-GEOD-37907 | biostudies-arrayexpress

CEA_SGF:E00010#bcr-abl

2005-05-01 | E-GEOD-1429 | biostudies-arrayexpress

RNA-Seq analysis of the WEHI-231-derived stable cell lines WEHI-control and WEHI-miR-148a

Project description:miRNAs regulate the expression of its targets genes by promoting mRNA degradation and translational repression. The goal of this study is to perform RNA-Seq in control or miR-148a-expressing WEHI-231 cell lines for the identification of miR-148a target genes. WEHI-control and WEHI-miR-148a cells were stimulated with anti-IgM (2 ug/ml) for 14 h. Total RNA was extracted, enriched for polyA-containing RNAs and submitted to RNA-Seq.

2016-02-22 | E-GEOD-75809 | biostudies-arrayexpress

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