Unknown,Transcriptomics,Genomics,Proteomics

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Gene Expression Profiling of the Calvaria from Conditional Hdac3 Defecient and Wild-type Mice

ABSTRACT: We utilized the Illumina MouseRef-8 gene expression technology to quantify differential gene expression between wildtype mice and mice with Osterix driven Cre conditional knockout of Hdac3 (Hdac3-CKO). We compared the RNA extracted from calvaria from 8 wildtype and 8 conditional knockout litter matched mice using two separate Illumina MouseRef-8 chips. Mice with exon 7 of Hdac3 flanked by loxP sites were crossed with mice expressing Cre driven by the Osterix promoter. RNA from 5 day old mouse calvarial explants (digested for 20 minutes with collagenase) was purified using TRIzol according to the manufacturerâs protocol (Invitrogen) and reverse transcribed using Qiagenâs Quantitect Reverse Transcription Kit. Two independent microarray experiments were performed; each experiment used RNA from four wildtype and four conditional knockout litter matched mouse calvaria.

ORGANISM(S): Mus musculus

SUBMITTER: Bridget Stensgard

PROVIDER: E-GEOD-21087 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Project description:Histone deacetylases (HDAC) are enzymes that modify key residues in histones to regulate chromatin architecture, and play a vital role in cell survival, cell cycle progression, and tumorigenesis. To understand the function of Hdac3, a critical component of the N-CoR/SMRT repression complex, a conditional allele of Hdac3 was engineered. Given the vital role of HDAC3 in normal cells and in the generation and treatment of various cancers, a conditional deletion of Hdac3 was engineered in mice. The deletion of Hdac3 in the germ line yielded very early embryonic lethality. Therefore, mouse embryonic-derived fibroblasts (MEFs) containing the Hdac3 conditional allele were used to examine the function of Hdac3 in cell viability and in cell cycle control. Given the links between Hdac3 and transcriptional repression, we used oligonucleotide micro arrays to examine RNA isolated from control and Cre recombinase expressing MEFs to define the changes in gene expression upon inactivation of Hdac3. Initially, we compared RNA from Ad-Cre infected Hdac3FL/+ and Hdac3FL/- MEFs and then we extended the analysis to Hdac3FL/- MEFs expressing Cre-ER (tamoxifen responsive Cre-estrogen receptor fusion protein). When the gene expression of ethanol-treated (vehicle) and tamoxifen-treated MEFs was compared at 72 hr post-induction, 83 genes were induced and 111 genes were down-regulated at least 1.5-fold upon inactivation of Hdac3. Approximately, 48 genes were up-regulated in both Ad-Cre and tamoxifen-treated MEFs at the 72 hr time point. The majority of the affected genes were associated with signal transduction and metabolism. Overall, few of the up-regulated genes at the 72hr time point in Ad-Cre and tamoxifen-treated MEFs are associated with apoptosis or with cell cycle control. Thus, these metabolic regulatory genes may be “core” Hdac3-regulated genes, and alterations in gene expression are unlikely to trigger apoptosis. Keywords: Conditional knock out analysis, genetic modification

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Gene Expression Profiling of the Calvaria from Conditional Hdac3 Defecient and Wild-type Mice

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