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The influence of the transcription factor EB for BCR-induced gene expression in human Ramos 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): Homo sapiens

PROVIDER: GSE212456 | GEO | 2024/06/25

REPOSITORIES: GEO

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

Project description: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

2024-06-25 | GSE212457 | GEO

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

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

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

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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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IKZF1 in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of IKZF1 in ALL, we isolated bone marrow cells from C57Bl6 mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with IKZF1-GFP or empty vector control (GFP) and subjected to gene expression analysis.

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Project description:In order to investigate the function of the adapterprotein Blnk in ALL, we isolated bone marrow cells from Blnk KO mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with Blnk-GFP or empty vector control (GFP) and subjected to gene expression analysis.

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Project description:In order to investigate the function of PAX5 in ALL, we isolated bone marrow cells from C57Bl6 mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with PAX5-GFP or empty vector control (GFP) and subjected to gene expression analysis.

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Role and function of STAT5 in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of STAT5 in ALL, we isolated bone marrow cells from STAT5 fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-GFP or empty vector control (GFP) and subjected to gene expression analysis.

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Role and function of Sox4 in BCR-ABL1 driven pre-B cells

Project description:In order to investigate the function of Sox4 in ALL, we isolated bone marrow cells from Sox4 fl/fl mice and transformed them with BCR-ABL1. In a second transduction the BCR-ABL1 driven pre-B cells were transformed either with CRE-ERT2 or empty vector control (ERT2) and subjected to gene expression analysis.

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