Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA136867 | ENA |
REPOSITORIES: ENA
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Project description:YY1 is a ubiquitously expressed transcription factor that has been demonstrated to be essential for pro-B cell development. However, the role of YY1 in other B cell populations has never been investigated. It has been proposed that YY1 is a key regulator for the germinal center B cell program since the YY1 motif was present in much higher frequency in germinal center B cell signature genes than signature genes of other B cell subsets. Indeed, in accord with this prediction, we demonstrated that deletion of YY1 by Cg1-Cre completely prevented differentiation of naïve B cells into germinal center B cells and plasma cells after antigen stimulation. To determine if YY1 was also required for the differentiation of other B cell populations, we deleted YY1 with CD19-Cre and found that all peripheral B cell subsets including B1 B cells require YY1 for their differentiation. By deleting YY1 acutely with ER-Cre, we demonstrated that all B cell subsets require YY1 for their maintenance. ChIP-seq shows that YY1 predominantly binds to promoters, and pathway analysis of the genes which bind YY1 show that they are enriched in ribosomal functions, mitochondrial functions such as bioenergetics, and functions related to transcription, such as mRNA splicing, metabolism of RNA. By RNA-seq analysis of differentially expressed genes, we demonstrated that YY1 normally activates genes involved in mitochondrial bioenergetics, while it normally downregulates genes involved in transcription, mRNA splicing, NF-kB signaling pathways, AP-1 transcription factor network, chromatin remodeling, cytokine signaling pathways, cell adhesion, cell proliferation and c-Myc targets.
2016-06-20 | GSE73532 | GEO
Project description:YY1 is a ubiquitously expressed transcription factor that has been demonstrated to be essential for pro-B cell development. However, the role of YY1 in other B cell populations has never been investigated. It has been proposed that YY1 is a key regulator for the germinal center B cell program since the YY1 motif was present in much higher frequency in germinal center B cell signature genes than signature genes of other B cell subsets. Indeed, in accord with this prediction, we demonstrated that deletion of YY1 by Cg1-Cre completely prevented differentiation of naïve B cells into germinal center B cells and plasma cells after antigen stimulation. To determine if YY1 was also required for the differentiation of other B cell populations, we deleted YY1 with CD19-Cre and found that all peripheral B cell subsets including B1 B cells require YY1 for their differentiation. By deleting YY1 acutely with ER-Cre, we demonstrated that all B cell subsets require YY1 for their maintenance. ChIP-seq shows that YY1 predominantly binds to promoters, and pathway analysis of the genes which bind YY1 show that they are enriched in ribosomal functions, mitochondrial functions such as bioenergetics, and functions related to transcription, such as mRNA splicing, metabolism of RNA. By RNA-seq analysis of differentially expressed genes, we demonstrated that YY1 normally activates genes involved in mitochondrial bioenergetics, while it normally downregulates genes involved in transcription, mRNA splicing, NF-kB signaling pathways, AP-1 transcription factor network, chromatin remodeling, cytokine signaling pathways, cell adhesion, cell proliferation and c-Myc targets.
2016-06-20 | GSE73531 | GEO
Project description:To investigate TFEB-dependent mRNA expression in murine B cells, FACS-sorted germinal center and non-germinal center B lymphocytes of B-cell-specific conditional TFEB KO mice and control littermates were subjected to RNA sequencing analysis
2024-06-25 | GSE237799 | GEO
Project description:Changes in DNA methylation are required for the formation of germinal centers (GC), but the mechanisms of such changes are poorly understood. Activation-induced cytidine deaminase (AID) has been recently implicated recently in DNA demethylation through its deaminase activity coupled with DNA repair. We investigated the epigenetic function of AID in vivo in germinal center B cells (GCB) isolated from wild type (WT) and AID-deficient (Aicda-/-) mice. We determined that the transit of B cells through the GC is associated with marked locus-specific loss of methylation and increased methylation diversity, both of which are lost in Aicda-/- animals. Differentially methylated cytosines (DMCs) between GCB and naïve B cells (NB) are enriched in genes that are targeted for somatic hypermutation (SHM) by AID and these genes form networks required for B cell development and proliferation. Finally, we observed significant conservation of AID-dependent epigenetic reprogramming between mouse and human B cells. ERRBS and RNA-seq of wild type and Aicda knockout murine naive and germinal center B cells. ERRBS of human naive and germinal center B cells
2015-09-15 | E-GEOD-71702 | biostudies-arrayexpress
Project description:Gene expression profiling of murine eGFP+ relfl/flCg1-Cre and eGFP− Cg1-Cre splenic germinal center B cells identifies genes regulated by the transcription factor c-REL in germinal center B cells.
2014-07-15 | GSE58839 | GEO
Project description:RNA-seq analysis of murine eGFP+ relbfl/flnfkb2fl/flCg1-Cre and Cg1-Cre splenic germinal center B cells identifies genes regulated by the transcription factors RELB and p52 (NF-kB2) in germinal center B cells.
2016-07-01 | GSE77374 | GEO
Project description:Gene expressions of murine germinal center and naive B cells on Affymetrix platform
2013-03-06 | GSE44260 | GEO
Project description:This study examined the loss of Foxp1 in B cells at different stages. RNA-seq was performed to examine gene expression differences fromB cells from wildtype and Foxp1 cKO spleens. We found strong enrichment for signatures related to down-regulation of immune responses, apoptosis and germinal center biology, including direct activation of Bcl6 and downregulation of Aicda/AID, the primary effector of SHM and CSR. These observations support a role for FOXP1 as a direct transcriptional regulator at key steps underlying B cell development in the mouse.
2019-09-17 | GSE137463 | GEO
Project description:True stem-like phenotypic plasticity is gradually lost during cellular differentiation due to the strengthening of epigenetic barriers. Here, we describe an unprecedented physiological gain of stem-like plasticity in germinal center B cells, that we termed “anaplasis”. Anaplasis was strictly dependent on help from T follicular helper cells and restricted to germinal center (GC) but not activated B cells, indicating both non- and cell-autonomous contributions to this phenotype. Anaplasis involved the transient reactivation of embryonic stem cell programs by T cell-responsive germinal center B cell transcription factors, suggesting an immunological functional checkpoint, that we show can be hijacked and even bypassed by specific lymphoma mutations. Anaplasis signatures were associated with unfavorable outcomes in B cell lymphomas, suggesting their contribution to tumor fitness. Altogether, we document a physiological re-acquisition of stem-like plasticity in germinal center B cells, which co-evolved with non cell-autonomous checkpoints linked to immune selection processes.
2025-10-29 | GSE298473 | GEO