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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. 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.

ORGANISM(S): Mus musculus

SUBMITTER: Hee-Woong Lim

PROVIDER: E-GEOD-42537 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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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

Gene expression in mouse liver depleted of HDAC3

Project description:Liver-specific depletion of HDAC3 leads to liver steatosis (fatty liver), suggesting disregulation of lipid metabolism. This is correlated with changes in lipid metabolic gene expression. Livers depleted of HDAC3 were removed from 12 week old male HDAC3 fl/fl mice (loxP sites flanking exon 4 to 7 of the HDAC3 gene encoding the catalytic domain of HDAC3) one week after the injection of AAV2/8-Tbg-Cre virus. Livers from the HDAC3 fl/fl mice injected with AAV2/8-Tbg-GFP were used as normal controls. mRNA was extracted from 100mg mouse liver samples and hybridized to Affymetrix microarrays. For each group (HDAC3 depleted liver and normal liver), we have 5 samples from different mice.

2011-03-11 | E-GEOD-25937 | 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

Gene expression profiling of liver-specific NCOR knockout mice

Project description:We profiled gene expression in livers depleted of NCOR (nuclear receptor corepressor) along with wild-type livers as control. NCOR floxed mice were intravenously injected with adeno-associated virus (AAV) expressing Cre or GFP. Livers were harvested at 2-weeks post-injection at 5pm (ZT10). Total RNA was extracted and hybridized to Affymetrx Mouse Gene 2.0 array.

2013-11-25 | E-GEOD-49387 | biostudies-arrayexpress

Gene expression profiling of HDAC3-depleted mouse liver rescued with wild-type exogenous HDAC3

Project description:We have shown that intravenous injection of HDAC3 floxed mice with adeno-associated virus (AAV) expressing Cre depletes hepatic HDAC3, upregulates lipogenic gene expression, and causes fatty liver. When AAV-Flag-HDAC3 wild-type (WT) is co-injected along with AAV-Cre, the exogenous HDAC3 is expressed at endogenous levels and can completely rescue fatty liver phenotype. Here we profile transcriptome of the rescued WT livers in comparison with HDAC3-depleted (KO) livers. 4-months old C57BL/6 male mice were co-injected with AAV-Cre or AAV-Cre plus AAV-Flag-HDAC3. Mice were fed ad libitum and harvested at 5 pm (ZT10) at 2-weeks post-injection. Liver total RNA was extracted and hybridized to Affymetrix Mouse Gene 1.0ST array.

2013-11-25 | E-GEOD-49386 | biostudies-arrayexpress

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.

2013-01-01 | GSE42537 | GEO

Gene expression profiles in mouse livers depleted of HDAC3 or NCOR1

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

2013-11-25 | E-GEOD-49388 | biostudies-arrayexpress

Expression data from mouse heart deficient of HDAC3

Project description:Gene expression changes in the heart of MCH3-KO mouse (HDAC3 f/f, Muscle Creatine Kinase-Cre) versus control WT mouse (HDAC3 f/f). Histone deacetylases (HDACs) play important roles in cardiac development and function. We show here that mice deficient of HDAC3 in heart and skeletabl muscle are relatively normal on normal chow, but develop hypertrophic cardiomyopathy and heart failure that leads to death on high-fat diet. This microarray experiment is to explore the underlying molecular mechanism. Hearts from 6-weeks old WT and MCH3-KO C57BL/6 mice (n=4 in each group, male) on normal chow were subjected to RNA extraction and Affymetrix Mouse Gene 1.0ST analysis.

2011-09-20 | E-GEOD-31251 | 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.

2013-01-01 | GSE42540 | GEO

Gene expression profiling in NCoR deficient mouse livers

Project description:The thyroid hormone receptor (TR) has been proposed to regulate target genes in the absence of triiodothyronine (T3), through the recruitment of the corepressors, NCoR and SMRT. NCoR and SMRT may thus play a key role in both hypothyroidism and resistance to thyroid hormone, though this has never been tested in vivo. To accomplish this we developed mice that express in the liver a NCoR protein (L-NCoR∆ID) that cannot interact with the TR. L-NCoR∆ID mice develop normally, however when made hypothyroid the repression of many positively regulated T3-target genes is abrogated, demonstrating that NCoR plays a specific and sufficient role in repression by the unliganded TR. Remarkably, in the euthyroid state, expression of many T3-targets are also upregulated in L-NCoR∆ID mice, demonstrating that NCoR also determines the magnitude of the response to T3 in euthyroid animals. While positive T3 targets were upregulated in L-NCoR∆ID mice in the hypo and euthyroid state there was less effect seen on negatively regulated T3 target genes. Thus, NCoR is a specific regulator of T3-action in vivo and mediates the activity of the unliganded TR. Furthermore, NCoR may play a key role in determining the differences in individual responses to similar levels of circulating T3. Keywords: NCoR, thyroid hormone signaling, mouse liver, DNA Microarray To better assess the role of NCoR in positive and negative regulation we performed micorarray analysis of gene expression in the livers of euthyroid and hypothyroid control and L-NCoR∆ID mice.

2008-12-03 | E-GEOD-10001 | biostudies-arrayexpress

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