Parts2014_GFPvar
Ontology highlight
ABSTRACT:
ORGANISM(S): Saccharomyces cerevisiae
SUBMITTER: Leopold Parts
PROVIDER: E-MTAB-2269 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
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Project description:Embryonic stem (ES) cells are isolated from the inner cell mass (ICM) of developing blastocysts, whereas epiblast stem cells (EpiSCs) are derived from the post-implantation epiblast and are characterized by a restricted developmental potential. Although certain mouse strains, such as the non-obese diabetic (NOD) mice, are considered “non-permissive” for ES cell derivation, they retain the capacity to generate EpiSCs. Using the NOD strain as a model, we characterized the stability of pluripotent states in cells generated by ICM explantation or direct in vitro reprogramming. We find that ES-like NOD stem cells can be captured in both approaches by providing exogenous constitutive expression of Klf4 or c-Myc transcription factors or small molecules that can replace these factors during in vitro reprogramming. The fully pluripotent NOD ES and iPS cells appear “metastable”, as the cells acquire an alternative EpiSC-like identity after removal of the exogenous factors, while reintroduction of these factors converts the cells back to ICM-like pluripotency. Our findings suggest that stem cells from different genetic backgrounds can assume distinct states of pluripotency in vitro, the stability of which is regulated by endogenous genetic determinants and can be modified by the continuous presence of defined exogenous factors. Gene expression profiling was performed in mouse ES, EpiSC and EpiSC-like cell lines.
2009-04-09 | E-GEOD-15603 | biostudies-arrayexpress
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2012-01-06 | E-GEOD-30279 | biostudies-arrayexpress
Project description:Induced pluripotent stem cells (iPSCs) are generated from somatic cells by the transduction of defined transcription factors and involves dynamic changes in DNA methylation. While the reprogramming of somatic cells is accompanied by de-methylation of pluripotency genes, the functional importance of de novo DNA methylation has not been clarified. Here, using loss-of-function studies, we generated iPSCs from fibroblasts that were deficient in de novo DNA methylation mediated by Dnmt3a and Dnmt3b. These iPSCs reactivated pluripotency genes, underwent self-renewal and showed restricted developmental potential which was rescued upon re-introduction of Dnmt3a and Dnmt3b. We conclude that de novo DNA methylation by Dnmt3a and Dnmt3b is dispensable for nuclear reprogramming of somatic cells. RNA levels of Dnmt3ab deficient iPSC cell lines were compared to control iPSC cell lines
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Project description:Transcriptional profiling of mouse lung tumors comparing Dnmt3a KO/K-ras G12D mutant with Dnmt3a WT/K-ras G12D mutant. The goal is to search for the difference of mRNA abundance between Dnmt3a KO and WT tumors. Two-condition experiment, KO vs. WT tissure. Biological replicates: 12.
2011-10-25 | E-GEOD-32415 | biostudies-arrayexpress
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Project description:Cervical cancer is a leading cause of cancer-related death in women worldwide. Nearly all cases of cervical cancer are attributed to infection with human papillomavirus (HPV), mainly high-risk type HPV16 and HPV18. Two viral genes, E6 and E7, play an important role in viral life cycle, since they delay keratinocyte differentiation and stimulate cell cycle progression, allowing the virus to exploit host DNA replication machinery to replicate its genome. Some of the oncogenic properties of E6 and E7 are mediated by host microRNAs (miRNAs) involved in the control of cell proliferation, senescence, and apoptosis. In order to identify genome-wide changes in miRNA expression profile, miRNA microarray analysis was performed on HFKs transduced with retroviral vectors carrying E6 and E7 genes of either HPV6 or HPV16 and with the LXSN empty vector. This dataset was used to identify and to further investigate the role of miR-146a-5p in cervical cancer.
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