Mus musculus
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA356733 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR5087560.fastq.gz | Fastqsanger.gz | |||
| SRR5087570.fastq.gz | Fastqsanger.gz | |||
| SRR5087580.fastq.gz | Fastqsanger.gz | |||
| SRR5087590.fastq.gz | Fastqsanger.gz | |||
| SRR5087600.fastq.gz | Fastqsanger.gz |
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Project description:Principles for the regulation of multiple developmental pathways by a versatile transcriptional factor, BLIMP1
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Project description:Principles for the regulation of multiple developmental pathways by a versatile transcriptional factor, BLIMP1 (RNA-Seq)
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Project description:To clarify the potential BLIMP1 downstream target regulating PD-L1 expression, we performed proteomics analysis using BLIMP1 Hep3B cells and control cells. Proteomics analysis revealed that SPI1 may serve as a pivotal transcriptional factor that enhances PD-L1 expression by acting as a downstream effector of BLIMP1.
2022-11-23 | PXD037621 | Pride
Project description:Tissue-resident memory T cells (Trm) are non-circulating memory T cells that localize to portals of pathogen entry such as the skin, gut and lung where they provide efficient early protection against reinfection. Trm are characterized by a molecular profile that actively prevents egress from peripheral sites including the constitutive expression of the lectin CD69 and down-regulation of the chemokine receptor (CCR)7 and sphingosine-1-phosphate receptor 1 (S1PR1). This program is partially mediated by down-regulation of the transcription factor KLF2; however, to date no transcriptional regulator specific to Trm has been identified. Here we show that the Blimp1 related transcription factor Hobit is specifically upregulated in Trm and together with Blimp1, mediates the development and maintenance of Trm in various tissues including skin, gut, liver and kidney. Importantly, we found that the Hobit/Blimp1 transcriptional module is also required for other tissue-resident lymphocytes including Natural Killer T (NKT) cells and liver tissue-resident NK cells (trNK). We show that these populations share a universal transcriptional program with Trm instructed by Hobit and Blimp1 that includes the repression of CCR7, S1PR1 and KLF2 thereby enforcing tissue retention. Our results identify Hobit and Blimp1 as major common regulators that drive the differentiation of distinct populations of tissue-resident lymphocytes.
2016-04-25 | GSE70813 | GEO
Project description:Humoral immunity requires the generation of high-affinity antibodies, which involves the generation of germinal centres (GC) promoting class switch and affinity maturation of antigen-specific B cells, and the differentiation of long-lived plasma cells. This multi-layered process is tightly controlled by the activity of a transcriptional network including Bcl6, essential for the development of GC, and Blimp1, required for the differentiation of plasma cells. Here, we reveal an additional layer of complexity by demonstrating that dynamic changes in E-protein activity mediated by Id3 govern both GC and plasma cell differentiation. We show that down-regulation of Id3 expression in B cells in essential for releasing E2A and E2-2, the combined activity of which is required for both GC B cell and plasma cell differentiation. We demonstrate that this pathway controls the expression of multiple key factors required for antigen-induced B cell differentiation, including Blimp1, Xbp1, Mef2b and CXCR4 and is therefore critical for establishing the transcriptional network that controls GC B cell and plasma cell differentiation. Genome binding of transcription factor E2A
2016-05-13 | E-GEOD-72828 | biostudies-arrayexpress
Project description:Transcription factors (TFs) regulate biological events depending on cellular contexts, precise mechanisms for which are elusive. BLIMP1 has been shown to play key roles in many developmental processes, canonically as a transcriptional repressor that targets to proximities of promoters. Here, we systematically and quantitatively characterized genomic binding patterns of BLIMP1 across four distinct, developing cell types; photoreceptor precursors, embryonic intestinal epithelium, plasmablasts, and primordial germ cells (PGCs). BLIMP1-binding sites are highly enriched in genomic regions proximal to transcription start sites (TSSs), majority of which are shared among cell types and are highly occupied by BLIMP1, whereas only a small number of associated genes are regulated consistently among cell types. In contrast, BLIMP1 weakly binds to more distal, cell type-specific sites with divergent recognition sequences, which account for gene regulations much more efficiently in proportion to the magnitude of expression level changes, with notably similar impacts per site among cell types. Various TF motifs contained in the cell type-specific binding sites exhibit only moderate impacts on transcription dynamics and BLIMP1-occupancy levels. On the other hand, germ cells uniquely involve the shared binding sites in the specification, and grossly maintain the binding pattern in late PGCs, accounting for vast majority of the repressive targets. Furthermore, we identified new sequence motifs strongly bound to BLIMP1 especially in the late PGCs, GGGAAA repeats, a few of which are located around key regulators of gametogenesis. These findings provide a foundation for understanding the genomic regulation of BLIMP1 across developmental processes.
2017-08-31 | GSE91040 | GEO
Project description:Transcription factors (TFs) regulate biological events depending on cellular contexts, precise mechanisms for which are elusive. BLIMP1 has been shown to play key roles in many developmental processes, canonically as a transcriptional repressor that targets to proximities of promoters. Here, we systematically and quantitatively characterized genomic binding patterns of BLIMP1 across four distinct, developing cell types; photoreceptor precursors, embryonic intestinal epithelium, plasmablasts, and primordial germ cells (PGCs). BLIMP1-binding sites are highly enriched in genomic regions proximal to transcription start sites (TSSs), majority of which are shared among cell types and are highly occupied by BLIMP1, whereas only a small number of associated genes are regulated consistently among cell types. In contrast, BLIMP1 weakly binds to more distal, cell type-specific sites with divergent recognition sequences, which account for gene regulations much more efficiently in proportion to the magnitude of expression level changes, with notably similar impacts per site among cell types. Various TF motifs contained in the cell type-specific binding sites exhibit only moderate impacts on transcription dynamics and BLIMP1-occupancy levels. On the other hand, germ cells uniquely involve the shared binding sites in the specification, and grossly maintain the binding pattern in late PGCs, accounting for vast majority of the repressive targets. Furthermore, we identified new sequence motifs strongly bound to BLIMP1 especially in the late PGCs, GGGAAA repeats, a few of which are located around key regulators of gametogenesis. These findings provide a foundation for understanding the genomic regulation of BLIMP1 across developmental processes.
2017-08-31 | GSE91038 | GEO
Project description:The transcription factor Blimp1 is not only an essential regulator of plasma cells, but also a risk factor for the development of autoimmune disease. Here, we demonstrate that the mouse Prdm1 (Blimp1) gene was partially activated at the chromatin and transcription level in early B cell development, although mature Prdm1 mRNA did not accumulate due to posttranscriptional regulation. By analyzing a mouse model that facilitated ectopic Blimp1 protein expression throughout B lymphopoiesis, we could demonstrate that Blimp1 impaired B cell development by interfering with the B cell gene expression program, while leading to an increased abundance of plasma cells by promoting premature plasmablast differentiation of immature and mature B cells. With progressive age, these mice developed an autoimmune phenotype characterized by the presence of autoantibodies and glomerulonephritis. Hence, these data identified ectopic Blimp1 expression as a novel mechanism that can explain how Blimp1 as a risk factor contributes to the development of autoimmune disease.
2018-11-30 | GSE111692 | GEO
Project description:We previously demonstrated by genomic and bioinformatical approaches that human macrophage (MΦ) activation is best described by a spectrum model (Xue et al, Immunity, 2014). MΦ integrate exogenous input signals on transcriptional level in a unique fashion to generate specific functional programs, enabling the plasticity in disease-related pathophysiologies. Such versatile responsiveness requires fast changes of transcription mediated by transcriptional regulators (TRs) or epigenomic changes. To better understand the principles of this regulation during human MΦ activation, we assessed histone modifications including H3K4me1, H3K4me3, H3K27me3, and H3K27Ac by ChIP-sequencing allowing us to characterize the functional state of promoters (active, poised, repressed) and enhancers (active, inactive, intermediate). Using transcriptome data from our MΦ spectrum model, we generated a co-regulation network of all TRs. Next, we overlaid epigenomic information and transcriptional changes of major TRs over time onto the TR network. We observed that input signals like IFNγ or TNFα induce a specific network of TRs that are transcriptionally regulated themselves, the combination of regulated TRs changes over time with a boost of transcriptional regulation of dozens of TRs 4 to 12 hrs post input signal exposure, almost all TRs within the network show active promoters, even if the TR itself is not expressed, and similar results are obtained for enhancers with open or at least intermediated states. These findings strongly suggest that in MΦ, the TR-defined cellular âswitch panelâ is always accessible thereby allowing MΦ to quickly respond to the diverse input signal repertoire from the environment. Epigenetic analysis of promoter and enhancer sites in primary human macrophage subtypes and correlation to RNA-seq expression data
2016-02-28 | E-GEOD-66593 | biostudies-arrayexpress
Project description:We previously demonstrated by genomic and bioinformatical approaches that human macrophage (MΦ) activation is best described by a spectrum model (Xue et al, Immunity, 2014). MΦ integrate exogenous input signals on transcriptional level in a unique fashion to generate specific functional programs, enabling the plasticity in disease-related pathophysiologies. Such versatile responsiveness requires fast changes of transcription mediated by transcriptional regulators (TRs) or epigenomic changes. To better understand the principles of this regulation during human MΦ activation, we assessed histone modifications including H3K4me1, H3K4me3, H3K27me3, and H3K27Ac by ChIP-sequencing allowing us to characterize the functional state of promoters (active, poised, repressed) and enhancers (active, inactive, intermediate). Using transcriptome data from our MΦ spectrum model, we generated a co-regulation network of all TRs. Next, we overlaid epigenomic information and transcriptional changes of major TRs over time onto the TR network. We observed that input signals like IFNγ or TNFα induce a specific network of TRs that are transcriptionally regulated themselves, the combination of regulated TRs changes over time with a boost of transcriptional regulation of dozens of TRs 4 to 12 hrs post input signal exposure, almost all TRs within the network show active promoters, even if the TR itself is not expressed, and similar results are obtained for enhancers with open or at least intermediated states. These findings strongly suggest that in MΦ, the TR-defined cellular â??switch panelâ?? is always accessible thereby allowing MΦ to quickly respond to the diverse input signal repertoire from the environment. Epigenetic analysis of promoter and enhancer sites in primary human macrophage subtypes and correlation to RNA-seq expression data
2016-02-28 | E-GEOD-66594 | biostudies-arrayexpress