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: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:B cells in the germinal center of the spleen produce antibodies in responses to different antigens. Tnfrsf13b knockout and A144E mice can underlie more aggressive B cells effector responses, possibly at the cost of inadvertent pathogenicity; however, neither the amplitude nor the pathogenicity are simple functions of the amount of antigen-specific IgG produced. We used microarrays to detail the global program of gene expression of germinal center B cells and identified distinct classes of up-regulated genes in the different strains of mice with Tnfrsf13b wild type, knockout, monoallilic or biallec A144E missense mutation.
2021-08-26 | GSE182739 | GEO
Project description:Id3 Orchestrates Germinal Center B Cell Development
| PRJNA329004 | ENA