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The miR-155/PU.1 axis acts on Pax5 to enable efficient terminal B cell differentiation [RNA-Seq]

ABSTRACT: miR-155 inhibits PU.1 expression, leading to the initiation of the initiation of plasma cell differentiation pathway. Additional PU.1 targets include a network of genes whose products are involved in adhesion, with direct links to B:T interactions.

ORGANISM(S): Mus musculus

PROVIDER: GSE61425 | GEO | 2014/09/26

SECONDARY ACCESSION(S): PRJNA261051

REPOSITORIES: GEO

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The miR-155/PU.1 axis acts on Pax5 to enable efficient terminal B cell differentiation [ChIP-Seq]

Project description:miR-155 inhibits PU.1 expression, leading to the initiation of the initiation of plasma cell differentiation pathway. Additional PU.1 targets include a network of genes whose products are involved in adhesion, with direct links to B:T interactions. Sequencing analysis of PU.1 binding in B cells using Illumina ChIP-seq sample prep kit and Illumina platform. Cells were from ex-vivo LPS and IL-4 activated (96h) splenic B cells from wild type, PU.1[155-/155-] and miR-155[-/-] mice.

2014-09-26 | E-GEOD-61424 | biostudies-arrayexpress

The miR-155/PU.1 axis acts on Pax5 to enable efficient terminal B cell differentiation [RNA-Seq]

Project description:miR-155 inhibits PU.1 expression, leading to the initiation of the initiation of plasma cell differentiation pathway. Additional PU.1 targets include a network of genes whose products are involved in adhesion, with direct links to B:T interactions. Sequencing analysis of B cell transcriptome using Illumina TruSeq mRNA sample prep kit and Illumina platform. RNA was isolated from ex-vivo LPS and IL-4 activated (96h) splenic B cells from wild type, PU.1[155-/155-] and miR-155[-/-] mice. 4-5 biological replicates per genotype and condition.

2014-09-26 | E-GEOD-61425 | biostudies-arrayexpress

The miR-155/PU.1 axis acts on Pax5 to enable efficient terminal B cell differentiation [ChIP-Seq]

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The miR-155-PU.1 axis acts on Pax5 to enable efficient terminal B cell differentiation.

Project description:A single microRNA (miRNA) can regulate the expression of many genes, though the level of repression imparted on any given target is generally low. How then is the selective pressure for a single miRNA/target interaction maintained across long evolutionary distances? We addressed this problem by disrupting in vivo the interaction between miR-155 and PU.1 in mice. Remarkably, this interaction proved to be key to promoting optimal T cell-dependent B cell responses, a previously unrecognized role for PU.1. Mechanistically, miR-155 inhibits PU.1 expression, leading to Pax5 down-regulation and the initiation of the plasma cell differentiation pathway. Additional PU.1 targets include a network of genes whose products are involved in adhesion, with direct links to B-T cell interactions. We conclude that the evolutionary adaptive selection of the miR-155-PU.1 interaction is exercised through the effectiveness of terminal B cell differentiation.

| S-EPMC4203942 | biostudies-literature

The miR-155/PU.1 axis acts on Pax5 to enable efficient terminal B cell differentiation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2014-09-25 | E-GEOD-61426 | biostudies-arrayexpress

The miR-155/PU.1 axis acts on Pax5 to enable efficient terminal B cell differentiation

Project description:This SuperSeries is composed of the SubSeries listed below.

2014-09-25 | GSE61426 | GEO

The hematopoietic master transcription factor PU.1 requires its interaction with the SWI/SNF remodeler to access chromatin de novo

Project description:PU.1 is a prototype master transcription factor (TF) of hematopoietic cell differentiation with diverse roles in different lineages. Analysis of its genome-wide binding pattern across PU.1 expressing cell types revealed manifold cell type-specific binding patterns. They are not consistent with the epigenetic and chromatin constraints to PU.1 binding observed in vitro, suggesting that PU.1 requires auxiliary factors to access DNA in vivo. Using a model of transient mRNA expression we show that PU.1 induction leads to the extensive remodeling of chromatin, redistribution of partner transcription factors and rapid initiation of a myeloid gene expression program in heterologous cell types. By probing PU.1 mutants for defects in chromatin access and screening for PU.1 proximal proteins in vivo, we found that its N-terminal acidic domain was required for the recruitment of SWI/SNF remodeling complexes, de novo chromatin access and stable binding as well as the redistribution of partner TFs.

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Project description:PU.1

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Project description:PU@LA Raw sequence reads

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Project description:Several studies have indicated an important role for miR-155 in the pathogenesis of B-cell lymphoma. Highly elevated levels of miR-155 were indeed observed in most B-cell lymphomas with the exception of Burkitt lymphoma (BL). However, the molecular mechanisms that underlie the oncogenic role of miR-155 in B-cell lymphoma are not well understood. To identify the miR-155 targets relevant for B-cell lymphoma, we performed RNA immunoprecipitation of Argonaute 2 in Hodgkin lymphoma (HL) cells upon miR-155 inhibition and in BL cells upon ectopic expression of miR-155. We identified 54 miR-155-specific target genes in BL cells and confirmed miR-155 targeting of DET1, NIAM, TRIM32, HOMEZ, PSIP1 and JARID2. Five of these targets are also regulated by endogenous miR-155 in HL cells. Both overexpression of miR-155 and inhibition of expression of the novel miR-155 target gene NIAM increased proliferation of BL cells. In primary B-cell lymphoma NIAM-positive cases have significant lower levels of miR-155 as compared to NIAM-negative cases, suggesting that NIAM is also regulated by miR-155 in primary B-cell lymphoma. Thus, our data indicate an oncogenic role for miR-155 in B-cell lymphoma which involves targeting the tumor suppressor NIAM.

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