Comparison of transcriptional changes in Cre infected with Vector infected alpha4-floxed MEFs
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE1708 | GEO | 2004/09/01
SECONDARY ACCESSION(S): PRJNA90633
REPOSITORIES: GEO
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Project description:To examine the transcriptional changes that occur following alpha4 deletion, RNA microarray analysis was performed using RNA from alpha4-floxed MEFs 48 hours after infection with the Cre-containing or Vector control virus.
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Project description:In this work, we aimed at studying the impact of microRNAs on antiviral responses, using inducible deletion of one or two copies of Dicer1 (in Dicer-floxed x EsrCRE+ MEFs). Unexpectedly, we discovered that Cre-ERT activation by hydroxytamoxifen (OHT) alone, independent of Dicer1 deletion, had a strong impact on antiviral responses. These microarrays were performed on SV40 immortalized Dicer1 fl/fl EsrCRE+ MEFs, Dicer1 fl/wt EsrCRE+ MEFs, 96 h after initial OHT treatment, and SV40 immortalized Dicer1 wt/wt EsrCRE+ MEFs, Dicer1 wt/wt EsrCRE-neg MEFs (Wild Type MEFs), 48 h after initial OHT treatment. These analyses revealed the strong induction of several antiviral genes (Rsad2, Cxcl10...), following Cre-ERT activation. SV40 immortalized mouse embryonic fibroblasts from various genotypes were stimulated 24h with 500nM hydroxytamoxifen, and further expanded for 24 or 72h. Each sample was analyzed on Agilent-028005 SurePrint G3 Mouse GE 8x60K Microarray Each sample is in simplicate - no biological replicates; sample 1-4 were processed/analyzed on a different microarray slide to 5-8 (different day/operator)
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Project description:Total gene expression analysis was performed on CRE induced conditional knockout E12.5 MEFs relative to GFP infected control MEFs. Intent was to analyze the role of H3f3b in overall gene expression. For conditional KO, three lines of H3f3b FL/FL E12.5 MEFs (cKO1, cKO2 and pcKO1) were transduced with Cre retroviruses and compared to their respective lines of MEFs transduced solely with GFP vector (as control). Total RNA was isolated for gene analysis.
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Project description:Comparison of transcriptional changes in Cre infected with Vector infected alpha4-floxed MEFs
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Project description:Histone acetyltransferases (HATs) GCN5/PCAF and CBP/p300 are transcription coactivators. However, how these HATs regulate ligand-induced nuclear receptor target gene expression remains unclear. Here we show in mouse embryonic fibroblasts (MEFs), deletion of GCN5/PCAF specifically eliminates acetylation on H3K9 (H3K9Ac) while deletion of CBP/p300 selectively reduces acetylation on H3K18 and H3K27 (H3K18/27Ac). Treating MEFs with a specific ligand for nuclear receptor PPARdelta induces sequential increases of H3K18/27Ac and H3K9Ac on the promoter of PPARdelta target gene Angptl4, which correlates with a robust ligand-induced Angptl4 expression. Inhibiting transcription elongation blocks ligand-induced H3K9Ac but not H3K18/27Ac on Angptl4 promoter. Finally, we show CBP/p300 and their HAT activities are required, while GCN5/PCAF and H3K9Ac are dispensable, for ligand-induced PPARdelta target gene expression in MEFs. These results highlight the substrate and site specificities of HATs in cells, and suggest that GCN5/PCAF- and CBP/p300-mediated histone acetylations play distinct roles in regulating ligand-induced nuclear receptor target gene expression. PCAF and GCN5 have some redundant function. To identify PCAF/GCN5-regulated genes, immortalized MEFs with PCAF knockout and GCN5 conditional knockout were infected with retroviruses expressing either Cre recombinase or vector alone. We prepared duplicated RNAs from either vector or Cre infected cells (PCAF-/-;GCN5+/- or PCAF-/-;GCN5+/-) and RNAs from either Vector or Cre infected the other independently immortalized cells for 6 affymetrix microarray.
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Project description:Cultured cancer cells exhibit substantial phenotypic heterogeneity when measured in a variety of ways such as sensitivity to drugs or the capacity to grow under various conditions. Among these, the ability to exhibit anchorage-independent cell growth (colony forming capacity in semisolid media) has been considered to be fundamental in cancer biology because it has been connected with tumor cell aggressiveness in vivo such as tumorigenic and metastatic potentials, and also utilized as a marker for in vitro transformation. Although multiple genetic factors for anchorage-independence have been identified, the molecular basis for this capacity is still largely unknown. To investigate the molecular mechanisms underlying anchorage-independent cell growth, we have used genome-wide DNA microarray studies to develop an expression signature associated with this phenotype. Using this signature, we identify a program of activated mitochondrial biogenesis associated with the phenotype of anchorage-independent growth and importantly, we demonstrate that this phenotype predicts potential for metastasis in primary breast and lung tumors. Keywords: c-Myc or v-Src retroviral vector-infected immortalized mouse embryonic fibroblasts. Expression data of c-Myc and v-Src transformed MEFs was used to validate an expression signature generated from human cultured breast cancer cell lines with anchorage-independent growth ability.
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