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BCL6 de-repression induces the fasting transcriptome and protects from steatosis (RNA-Seq)

ABSTRACT: Here, we find that the B cell lymphoma 6 (BCL6) repressor is enriched upon feeding and converges genome-wide with PPARs to opposingly control lipid metabolism.

ORGANISM(S): Mus musculus

PROVIDER: GSE118787 | GEO | 2019/04/16

REPOSITORIES: GEO

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BCL6 de-repression induces the fasting transcriptome and protects from steatosis (ChIP-Seq II)

Project description:Here, we find that the B cell lymphoma 6 (BCL6) repressor is enriched upon feeding and converges genome-wide with PPARs to opposingly control lipid metabolism.

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BCL6 de-repression induces the fasting transcriptome and protects from steatosis (ChIP-Seq I)

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BCL6 de-repression induces the fasting transcriptome and protects from steatosis

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BCL6 de-repression induces the fasting transcriptome and protects from steatosis

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

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BCL6 de-repression induces the fasting transcriptome and protects from steatosis (RNA-Seq)

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Dynamic repression by BCL6 controls the genome-wide liver response to fasting and steatosis.

Project description:Transcription is tightly regulated to maintain energy homeostasis during periods of feeding or fasting, but the molecular factors that control these alternating gene programs are incompletely understood. Here, we find that the B cell lymphoma 6 (BCL6) repressor is enriched in the fed state and converges genome-wide with PPARα to potently suppress the induction of fasting transcription. Deletion of hepatocyte Bcl6 enhances lipid catabolism and ameliorates high-fat-diet-induced steatosis. In Ppara-null mice, hepatocyte Bcl6 ablation restores enhancer activity at PPARα-dependent genes and overcomes defective fasting-induced fatty acid oxidation and lipid accumulation. Together, these findings identify BCL6 as a negative regulator of oxidative metabolism and reveal that alternating recruitment of repressive and activating transcription factors to shared cis-regulatory regions dictates hepatic lipid handling.

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Cooperative transcriptional repression by BCL6 and BACH2 in germinal center B-cell differentiation

Project description:The transcriptional repressors BCL6 and BACH2 are crucial regulators of germinal center (GC) B-cell fate, and are known to interact and repress transcription of PRDM1, a key driver of plasma cell differentiation. How these factors cooperate is not fully understood. Herein we show that while GC formation is only minimally impaired in Bcl6+/- or Bach2+/- mice, double heterozygous Bcl6+/-Bach2+/- mice exhibit profound reduction in GC formation. Splenic B-cells from Bcl6+/- Bach2+/- mice display accelerated plasmacytic differentiation and high expression of key plasma cell genes such as Prdm1, Xbp1 and CD138. ChIP-seq revealed that in B-cells BACH2 is mostly bound to genes together with its heterodimer partner MAFK. The BACH2-MAFK complex binds to sets of genes known to be involved in the GC response, 60% of which are also targets of BCL6. Approximately 30% of BACH2 peaks overlap with BCL6 including cis-regulatory sequences of the PRDM1 gene. BCL6 also modulates BACH2 protein stability and their protein levels are positively correlated in GC B-cells. Therefore, BCL6 and BACH2 cooperate to orchestrate gene expression patterning in GC B cells through both transcriptional and biochemical mechanisms, which collectively determine the proper initiation and timing of terminal differentiation. ChIP-seq using P18 antibodies in OCI-Ly7 cells

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