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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.

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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.

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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.

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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

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

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