Project description:To investigate the role of the transcriptional repressor Rev-erb alpha in epididymal white adipose tissue, we performed a microarray analysis of gene expression in the epididymal white adipose tissue of wildtype and Rev-erb alpha knock-out mice. Examination of the transcriptome in epididymal white adipose tissue of Rev-erb alpha kockout mice compared to wildtype mice.
Project description:The goal of this study is to identify the cistrome of the transcriptional repressor Rev-erb alpha in epididymal white adipose tissue. Performing Rev-erb alpha ChIP-seq on epididymal white adipose tissue from wildtype mice at 5PM when Rev-erb alpha protein level peaks in wild type (WT) mice, we were able to globally determine the genomic regions undergoing Rev-erb alpha-dependent de-repression. Examination of Rev-erb alpha binding in epididymal white adipose tissue.
Project description:The goal of this study is to identify the cistrome of the transcriptional repressor Rev-erb alpha in epididymal white adipose tissue. Performing Rev-erb alpha ChIP-seq on epididymal white adipose tissue from wildtype mice at 5PM when Rev-erb alpha protein level peaks in wild type (WT) mice, we were able to globally determine the genomic regions undergoing Rev-erb alpha-dependent de-repression.
Project description:To investigate the role of the transcriptional repressor Rev-erb alpha in epididymal white adipose tissue, we performed a microarray analysis of gene expression in the epididymal white adipose tissue of wildtype and Rev-erb alpha knock-out mice.
Project description:Based upon integrated analysis of transcriptomes and cistromes in Rev-erb alpha knock-out mice, we found that beta-Klotho (KLB) mRNA and protein are markedly induced in white adipose tissue but not in brown adipose tissue or liver of mice lacking Rev-erb alpha. In order to address the mechanism of the tissue-specific regulation of Klb transcription by Rev-erb apha, we performed global run-on followed by high-throughput sequencing (GRO-seq) to measure nascent transcription in different tissues in wildtype mice and Rev-erb alpha knock-out mice.
Project description:We have reported that cold temperature challenge results in a dramatic decrease in levels of the transcriptional repressor, Rev-erb alpha. Performing Rev-erb alpha ChIP-seq on brown adipose from wildtype animals kept at thermoneutrality or cold-challenged (and using Rev-erb alpha KO brown adipose as a control), we were able to globally determine the genomic regions undergoing Rev-erb alpha-dependent de-repression.
Project description:This SuperSeries is composed of the following subset Series: GSE34018: Integral roles for Rev-erb alpha and Rev-erb beta in the circadian clock function [Expression array] GSE34019: Integral roles for Rev-erb alpha and Rev-erb beta in the circadian clock function [ChIP_seq] Refer to individual Series
Project description:We report the genomic regions enriched for Rev-erb(beta) binding in WT mouse liver, in addition to the false positive regions enriched by ChIP for Rev-erb(alpha) in Rev-erb(alpha) KO liver. In conjunction with previously published data for Rev-erb(alpha) in GSE26345 (GSM647029, GSM647033, and GSM647034), we report the common and subtype specific cistromes for Rev-erb using a quantitative analysis method.
Project description:The circadian clock acts at the genomic level to coordinate internal behavioral and physiologic rhythms via the CLOCK-BMAL transcriptional heterodimer. Although the nuclear receptors REV-ERB? and ? have been proposed to contribute to clock function, their precise roles and importance remain unresolved. To establish their regulatory potential we generated comparative cistromes of both Rev-erb isoforms, which revealed shared recognition at over ~50% of their total sites and extensive overlap with the master clock regulator Bmal. While Rev-erb? has been shown to directly regulate Bmal expression, the cistromic analysis reveals a more profound connection between Bmal and Rev-erb? and ? regulatory circuits than previously suspected. Genes within the intersection of the Bmal and Rev-erb cistromes are highly enriched for both clock and metabolic functions. As predicted by the cistromic analysis, dual depletion of Rev-erb?/? function by creating double-knockout mice (DKOs) profoundly disrupted circadian expression of core clock and lipid homeostatic genes. As a result, DKOs show strikingly altered circadian wheel-running behavior and deregulated lipid metabolism. These data reveal an integral role of Rev-erb?/? in clock function as well as provide a cistromic basis for the integration of circadian rhythm and metabolism. Total RNA was obtained from livers of wild-type and Liver-specific Reverb alpha/beta double knockout mice at ZT 0, 4, 8, 12, 16, and 20.
Project description:The circadian clock acts at the genomic level to coordinate internal behavioral and physiologic rhythms via the CLOCK-BMAL transcriptional heterodimer. Although the nuclear receptors REV-ERBα and β have been proposed to contribute to clock function, their precise roles and importance remain unresolved. To establish their regulatory potential we generated comparative cistromes of both Rev-erb isoforms, which revealed shared recognition at over ~50% of their total sites and extensive overlap with the master clock regulator Bmal. While Rev-erbα has been shown to directly regulate Bmal expression, the cistromic analysis reveals a more profound connection between Bmal and Rev-erbα and β regulatory circuits than previously suspected. Genes within the intersection of the Bmal and Rev-erb cistromes are highly enriched for both clock and metabolic functions. As predicted by the cistromic analysis, dual depletion of Rev-erbα/β function by creating double-knockout mice (DKOs) profoundly disrupted circadian expression of core clock and lipid homeostatic genes. As a result, DKOs show strikingly altered circadian wheel-running behavior and deregulated lipid metabolism. These data reveal an integral role of Rev-erbα/β in clock function as well as provide a cistromic basis for the integration of circadian rhythm and metabolism. Identification of Reverb alpha and Reverb beta binding sites in mouse liver at ZT8