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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE42540 | GEO | 2013/01/01

SECONDARY ACCESSION(S): PRJNA182239

REPOSITORIES: GEO

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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.

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Project description:The histone deacetylase HDAC3 is associated with the NCoR/SMRT co-repressor complex and its canonical function is in transcriptional repression, but it can also activate transcription. Here we show that the repressor and activator functions of HDAC3 can be genetically separated in Drosophila. A lysine substitution in the N-terminus (K26A) disrupts its catalytic activity and activator function, whereas a combination of substitutions (HEBI) abrogating the interaction with SMRTER enhance repressor activity beyond wild-type in the early embryo. We conclude that the critical functions of HDAC3 in embryo development involve catalytic-dependent gene activation and non-enzymatic repression by several mechanisms, including tethering of loci to the nuclear periphery.

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