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Nuclear Receptor Corepressors are Required for the Histone Deacetylase Activity of HDAC3 In Vivo (Microarray)

ABSTRACT: We report the hepatic gene expression changes in NCOR and SMRT DADm-mutated mice.

ORGANISM(S): Mus musculus

PROVIDER: GSE42537 | GEO | 2013/01/01

SECONDARY ACCESSION(S): PRJNA182232

REPOSITORIES: GEO

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Nuclear Receptor Corepressors are Required for the Histone Deacetylase Activity of HDAC3 In Vivo (Microarray)

Project description:We report the hepatic gene expression changes in NCOR and SMRT DADm-mutated mice. 10-12 wk male mouse liver for RNA extraction and hybridization on Affymetrix microarrays. We sought to find differential gene changes between wt and NS-DADm mice.

2013-01-01 | E-GEOD-42537 | biostudies-arrayexpress

Nuclear Receptor Corepressors are Required for the Histone Deacetylase Activity of HDAC3 In Vivo (ChIP-Seq)

Project description:We report the genomic regions enriched in Histone Deacetylase 3 (HDAC3) in mouse livers. We also report the change of HDAC3 occupancy upon DAD mutations in NCOR and SMRT. HDAC3 enriched genomic regions in WT and NS-DADm mice livers using Illumina GAIIx.

2013-01-01 | E-GEOD-42540 | biostudies-arrayexpress

Nuclear Receptor Corepressors are Required for the Histone Deacetylase Activity of HDAC3 In Vivo

Project description:Histone deacetylase 3 (HDAC3) is an epigenome-modifying enzyme that is required for normal mouse development and tissue-specific functions. In vitro, HDAC3 protein itself has minimal enzyme activity, but gains its histone deacetylation function from stable association with the conserved deacetylase activation domain (DAD) contained in nuclear receptor corepressors NCOR1 and SMRT. Here we show that HDAC3 enzyme activity is undetectable in mice bearing point mutations in the DAD of both NCOR1 and SMRT (NS-DADm), despite normal levels of HDAC3 protein. Local histone acetylation is increased, and genomic HDAC3 recruitment is reduced though not abrogated. Remarkably, the NS-DADm mice are born and live to adulthood, whereas genetic deletion of HDAC3 is embryonic lethal. These findings demonstrate that nuclear receptor corepressors are required for HDAC3 enzyme activity in vivo, and suggest that a deacetylase-independent function of HDAC3 may be required for life. This SuperSeries is composed of the SubSeries listed below. Refer to individual Series.

2013-01-01 | E-GEOD-42541 | biostudies-arrayexpress

Nuclear Receptor Corepressors are Required for the Histone Deacetylase Activity of HDAC3 In Vivo

2013-01-01 | GSE42541 | GEO

Nuclear Receptor Corepressors are Required for the Histone Deacetylase Activity of HDAC3 In Vivo (ChIP-Seq)

Project description:We report the genomic regions enriched in Histone Deacetylase 3 (HDAC3) in mouse livers. We also report the change of HDAC3 occupancy upon DAD mutations in NCOR and SMRT.

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Nuclear receptor corepressor (NCOR) and HDAC3 in hypothalamus [ChIP-Seq]

Project description:We determined genomic binding of HDAC3 in mouse hypothalamus by ChIP-seq, and identified target genes of the NCOR/HDAC3 complex in hypothalamus of NS-DADm (mutated deacetylase activation domain in NCORs) mice by RNA-seq.

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Nuclear receptor corepressor (NCOR) and HDAC3 in hypothalamus [RNA-Seq]

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The HDAC3 Enzymatic Activity Regulates Skeletal Muscle Fuel Metabolism

Project description:We address whether the functions of HDAC3 in skeletal muscle require its enzyme activity. By mutating the NCoR/SMRT corepressors in a knock-in mouse model named NS-DADm, we ablated the enzymatic activity of HDAC3 without affecting its protein levels. Compared to the control mice, skeletal muscles from NS-DADm mice showed lower force generation, enhanced fatigue resistance, enhanced fatty acid oxidation, reduced glucose uptake during exercise, upregulated expression of metabolic genes involved in branched-chain amino acids (BCAAs) catabolism, and aging-associated reduction in muscle mass, without changes in the muscle fiber type composition or mitochondrial protein content. These findings demonstrate that the metabolic function of HDAC3 in skeletal muscles requires its enzymatic activity.

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HDAC3 ensures stepwise epidermal stratification via NCoR/SMRT-reliant mechanisms independent of its histone deacetylase activity (HDAC3 NCoRSMRT microarray)

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HDAC3 ensures stepwise epidermal stratification via NCoR/SMRT-reliant mechanisms independent of its histone deacetylase activity (HDAC3_KLF4_ChIPseq)

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