Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA190687 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Dnmt3L-dependent regulation of DNA methylation promotes stem cells differentiation toward primitive germinal cells
| PRJNA190684 | ENA
Project description:Dnmt3L-dependent regulation of DNA methylation promotes stem cells differentiation toward primitive germinal cells [MeDIP-seq]
| PRJNA190686 | ENA
Project description:Dnmt3L-dependent regulation of DNA methylation promotes stem cells differentiation toward primitive germinal cells [ChIP-seq]
| PRJNA213234 | ENA
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
Project description:BRG1-dependent regulation of Tceal7 promotes myoblast differentiation
| PRJNA1423131 | ENA
Project description:Comparison of gene expression differences between Dnmt3L heterozygous and wildtype pachytene spermatocytes, and similarly between Dnmt3L heterozygous and wildtype round spermatids which were isolated from the Dnmt3L knockout mouse line. This array was conducted to address the hypothesis that Dnmt3L heterozygosity results in deregulated gene expression within spermatocytes and spermatids. Results show that Dnmt3L heterozygosity causes numerous genes to be differentially regulated on a genome-wide level, showing that DNMT3L has an important role in regulating gene expression within these male germ cells.
2011-03-01 | GSE20241 | GEO
Project description:DNA methylation is essential for mammalian development. Studies of the catalytically inactive DNA methyltransferase Dnmt3l have mainly been limited to mice where Dnmt3l was shown to be essential for fertility, de novo DNA methylation in early embryos and maintenance of DNA methylation patterns in mouse pluripotent stem cells. Recent work revealed that DNMT3L is the most highly enriched chromatin factor in naive human pluripotent stem cells (hPSCs) compared with primed hPSCs. Stem cell-based human embryo models and naive hPSCs provide a unique opportunity to functionally dissect human developmental mechanisms. Here we use naive hPSCs and human blastoids, a 3D human blastocyst model, to investigate the functional impact of DNMT3L on human naive pluripotency and preimplantation development. We demonstrate an essential role of DNMT3L in trophectoderm cell fate induction, maintenance of DNA methylation patterns and chromatin states in naive hPSCs, and blastoid lineage identity. We further show that DNMT3L promotes reprogramming to naive pluripotency, and has integrated a hominoid-specific naive human pluripotency gene regulatory program involving evolutionary recent transposable elements. Therefore, DNMT3L plays conserved and hominoid-specific functions in human naive pluripotency and pre-implantation development.
2026-08-25 | PXD055233 | Pride
Project description:The roles of translational control in the immune system are poorly understood. In this study, we performed CRISPR/Cas9-mediated functional screening of RNA helicases in an in vitro system of plasma cell differentiation and identified Dhx29 as a critical regulator of this process. Mice with B cell-specific deletion of Dhx29 exhibited severely impaired germinal center B cell formation, plasma cell differentiation, and antibody production. Mechanistically, Dhx29 promotes translation of Tcf3 and Tle3 via binding to 5’UTRs of those mRNAs. In the absence of Dhx29, B cells exhibit normal proliferation but fail to undergo class switch to IgG1 and differentiation into plasma cells, resulting in impaired antibody production. Ectopic expression of TCF3 and Tle3 largely restores plasma cell differentiation of Dhx29-deficient B cells. Therefore, this study unravels critical roles of Dhx29 in promoting translation of key transcription factors controlling germinal center response and plasma cell differentiation, discovers a previously unrecognized role of Tle3 in plasma cell differentiation, and illustrates the functional importance of translation control in the immune system.
2026-08-24 | PXD073591 | Pride
Project description:Serum response factor (SRF) is a transcription factor essential for cell proliferation, differentiation, and migration, and is required for primitive streak and mesoderm formation in the embryo. The canonical roles of SRF are mediated by a diverse set of context-dependent cofactors. Here we show that SRF physically interacts with CTCF and cohesin subunits at TAD boundaries and loop anchors. SRF reinforces the insulation of TADs and promotes the formation of long-range chromatin loops. In ES cells, SRF associates with Oct4, Sox2, and Nanog and contributes to the formation of 3D pluripotency hubs. Our findings reveal new roles of SRF in higher-order chromatin organization.
2024-10-14 | PXD049365 | Pride
Project description:Klhl6 belongs to the KLHL gene family, which is composed of an N-terminal BTB-POZ domain and 4 to 6 Kelch motifs in tandem. Several of these proteins function as adaptors of the Cullin3 E3 ubiquitin ligase complex. Here we report that Klhl6 deficiency induces, as previously described, a two-fold reduction in mature B cells. However, we find that this deficit is centered on the inability of transitional T1 B cells to survive and to progress toward the T2 B cell stage, whereas cells that have passed this step generate normal germinal centers upon a T-dependent immune challenge. Klhl6-deficient T1 B cells showed a two-fold over-expression of genes linked with cell proliferation, including most targets of the APC/C complex, a set of genes whose expression is precisely down-modulated upon culture of splenic transitional B cells in presence of BAFF. These results thus suggest a delay in the differentiation process of Klhl6-deficient B cells between the immature and transitional stage. We further show, in the BL2 Burkitt’s lymphoma cell line, that KLHL6 interacts with Cullin3, but also that it binds to HBXIP/Lamtor5, a protein involved in cell cycle regulation and cytokinesis. Finally, we report that KLHL6, which is recurrently mutated in B cell lymphomas, is an off-target of the normal somatic hypermutation process taking place in germinal center B cells in both mice and humans, thus leaving open, whether, in spite of the lack of impact of Klhl6 deficiency on germinal center B cell expansion, mutants could contribute to the oncogenic process.
2018-07-17 | E-MTAB-5928 | biostudies-arrayexpress