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E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells

ABSTRACT: This SuperSeries is composed of the following subset Series: GSE32353: Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells (nCounter) GSE32354: Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null liver (Affymetrix) Refer to individual Series

ORGANISM(S): Mus musculus

SUBMITTER: Madhu Ouseph

PROVIDER: E-GEOD-32355 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells (nCounter)

Project description:To understand the underlying cause and mechanisms of changes in hepatocyte ploidy upon Albumin-Cre mediated deletion of E2f7&8 and Mx1-Cre mediated deletion of E2f1,2&3 and germline deleted trophoblast giant cells, we analysed global gene expression of 6 weeks and 2 months liver tissues. RNA was extracted from liver tissues using trizol method and Arcturus PicoPure RNA Isolation Kit for laser capture microdisected trophoblast giant cells. Gene deletion in samples confirmed by PCR genotyping of DNA isolated from each sample.

2012-08-31 | E-GEOD-32353 | biostudies-arrayexpress

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Project description:Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null liver (Affymetrix)

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Expression data from E2f7/E2f8/E2f3a null placentas and embryos

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Project description:E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells

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Expression data from E2f7/E2f8/E2f3a null placentas and embryos

Project description:To understand the underlying cause and mechanisms of embryonic lethality observed in combined loss of E2f7 and E2f8, we compared global gene expression profiles of wild type, germline deleted and sox2-Cre/Cyp19-Cre deleted embryos and placentas. RNA was extracted from E10.5 embryos and placentas. Gene deletion in samples confirmed by PCR genotyping of DNA isolated from each sample.

2012-08-31 | E-GEOD-30488 | biostudies-arrayexpress

Mus musculus

Project description:Expression data from E2f7/E2f8 and E2f1/E2f2/E2f3 null and wild type liver along with E2f7/E2f8 null and wild type trophoblast giant cells (nCounter)

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Transcriptomes of E2F7/8 DKO liver tumors

Project description:E2F transcriptional activators and repressors regulate cell cycle-dependent gene expression. Using a series of E2f loss- and gain-of-function mice we show that development is relatively insensitive to alterations in individual E2F levels and composition. However, modest increases in E2F transcriptional output (E2f7Δ/Δ;E2f8Δ/Δ, E2f1KI/1KI and E2f3bKI/3bKI) resulted in spontaneous hepatocellular carcinoma (HCC) without additional organ involvement, whereas decreases (E2f1-/- and E2f3b-/-) protected against HCC. DNA binding domain-, cell type- and temporal-specific gene ablation strategies defined a cell autonomous oncogenic role for E2F1/3B and a tumor suppressor role for E2F8 in hepatocytes during early post-natal liver development. Chromatin binding and expression profiling revealed a mechanism involving activation by E2F1/3B and repression by E2F7/8 to antagonistically regulate a common set of target genes associated with HCC progression. Thus, while development is sufficiently robust to withstand changes in E2F composition and activity, the liver is uniquely sensitive to perturbations in E2Fs. In summary, precise E2F transcriptional output in hepatocytes during early adolescence is critical to foster a cancer-free life span.

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Transcription profiling of mouse small intestines

Project description:Rb and E2F are thought to play antagonistic roles in celll proliferation. However, this model is based mostly from in vitro cell culture systems. We used small intestines to test this model in vivo. We found that deletion of E2f1-3 in the small intestine of mice suppressed the ectopic expression of E2F targets and cell proliferation caused by Rb-deficiency. Surprisingly, E2f1-3 deletion failed to arrest the proliferation of intestinal cells containing an intact Rb gene, and instead led to E2F target derepression and apoptosis. Experiment Overall Design: Total RNA of crypts and villi from wild-type, Rb-/-, E2f1-/-, E2f2-/-, E2f3-/-, E2f1-/-, E2f2-/-, and E2f3-/- small intestines. Small intestines were harvested 7 days after mice were injected intraperitoneally with beta-napthoflavone.

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MMTV-Myc tumor development in E2F-null backgrounds

Project description:Advances in genomic signatures have begun to dissect breast cancer heterogeneity, and application of these signatures will allow the prediction of which pathways are important in tumor development. Here we used genomic signatures to predict involvement of specific E2F transcription factors in Myc-induced tumors. We genetically tested this prediction by interbreeding Myc transgenics with mice lacking various activator E2F alleles. Tumor latency decreased in the E2F1 mutant background and significantly increased in both the E2F2 and E2F3 mutants. Investigating the mechanism behind these changes revealed a reduction in apoptosis in the E2F1 knockout strain. E2F2 and E2F3 mutant backgrounds alleviated Myc effects on the mammary gland, reducing the susceptible tumor target population. Gene expression data from tumors revealed that the E2F2 knockout background resulted in fewer tumors with EMT, corresponding with a reduction in probability of Ras activation. In human breast cancer we found that a low probability of E2F2 pathway activation was associated with increased relapse-free survival time. Together these data illustrate the predictive utility of genomic signatures in deciphering the heterogeneity within breast cancer and illustrate the unique genetic requirements for individual E2Fs in mediating tumorigenesis in both mouse models and human breast cancer. MMTV-Myc tumors were generated in an E2F wild-type, E2F1 null, E2F2 null and E2F3 heterozygous background. When the primary tumor reached the endpoint, the tumors were flash frozen. 20 tumors from each genotype were selected for microarray analysis.

2011-12-29 | E-GEOD-24594 | biostudies-arrayexpress

Expression data from lenses triply deficient for E2F1, E2F2, and E2F3 transcription factors

Project description:The E2F family consists of transcriptional repressors and activators that control cell proliferation. In the classic paradigm of cell cycle regulation, the three activators, E2F1, E2F2 and E2F3, are invariably depicted as the final components of a CDK/Rb signaling cascade that executes the transcriptional program necessary to commit cells to enter S phase. Unexpectedly, we find through analysis of Affymetrix expression array data that mature lens epithelial cells deficient for E2F1-3 fail to repress cell cycle-regulated genes (and other targets of E2F) and that this corresponds with subsequent apoptosis and cellular collapse in the lens. Murine lenses were collected at two stages of development for RNA extraction and hybridization on Affymetrix microarrays. Our aim was to determine key events that lead to cellular collapse of lenses triply deficient for E2F1, E2F2, and E2F3 in neonates.

2010-06-23 | E-GEOD-16533 | biostudies-arrayexpress

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