Stella
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Project description:Oocyte acquires developmental competence during its maturation. This stage is accompanied with large-scale alteration in transcription, and series of genome-wide epigenetic reprogramming, including de novo establishment of DNA methylation. However, our understanding of mechanisms regulating this process is limited. To investigate the role of Stella (Dppa3) in de novo methylation during mouse oogenesis, here we measured DNA methylation by RRBS and expression profiles by RNA-seq in PGCs and oocytes at serveral development stages, including genotypes of both Stella (Dppa3) +/- and Stella -/-.
2018-09-24 | GSE78149 | GEO
Project description:The maternal-to-zygotic transition (MZT) marks the period when the embryonic genome is activated and acquires control of development. Maternally inherited factors play a key role in this critical developmental process, which occurs at the 2-cell stage in mice. Here we investigated the function of the maternally inherited factor STELLA (DPPA3) using single-cell/embryo approaches. This submission concerns itself with transcriptional profiling of wild type and Stella knockout (Stella-/-) oocytes, wild type and Stella maternal/zygotic knockout (StellaM/Z-/-) 1-cell and 2-cell embryos. We show that loss of maternal STELLA results in widespread transcriptional mis-regulation and a partial failure of MZT. Strikingly, activation of the LTR class of transposable elements (TE), and particularly 2-cell specific MuERV-L elements, is significantly impaired in StellaM/Z-/- embryos, which leads to a failure to upregulate selected chimeric transcripts. We propose that STELLA is involved in ensuring activation of TEs that themselves play a key role during early development, in part through regulating embryonic gene expression.
2017-03-22 | E-MTAB-5210 | biostudies-arrayexpress
Project description:Global DNA hypomethylation and DNA hypermethylation of promoter regionsâincluding tumor suppressor genesâare frequently detected in human cancers. Although many studies have suggested a contribution to carcinogenesis, it is still unclear whether the aberrant DNA hypomethylation observed in tumors is a consequence or a cause of cancer. We found that overexpression of Stella (also known as PGC7, Dppa3), a maternal factor required for the maintenance of DNA methylation in early embryos, induced global DNA hypomethylation and transformation in NIH3T3 cells. This hypomethylation was due to the binding of Stella to Np95 (also known as Uhrf1, ICBP90) and the subsequent impairment of Dnmt1 localization. In addition, enforced expression of Stella enhanced the metastatic ability of B16 melanoma cells through the induction of metastasis-related genes by inducing DNA hypomethylation of their promoter regions. Such DNA hypomethylation itself causes cellular transformation and metastatic ability. These data provide new insight into the function of global DNA hypomethylation in carcinogenesis. We used microarrays to detail the global programme of gene expression by PGC7/Stella overexpression. RNA was extracted from NIH3T3 or B16F10 murine cell lines overexpressed PGC7/Stella and was hybridized on Affymetrix microarrays. We compared gene expression levels between control and PGC7/Stella-overexpressed cells. Microarray analysis was performed in NIH3T3 cells including two independent Stella-expressing NIH3T3 clones and a mixture of Stella-expressing NIH3T3 clones and in B16-F10 cells including three independent Stella-expressing B16-F10 clones.
2016-05-13 | E-GEOD-68837 | biostudies-arrayexpress
Project description:Global DNA hypomethylation and DNA hypermethylation of promoter regions—including tumor suppressor genes—are frequently detected in human cancers. Although many studies have suggested a contribution to carcinogenesis, it is still unclear whether the aberrant DNA hypomethylation observed in tumors is a consequence or a cause of cancer. We found that overexpression of Stella (also known as PGC7, Dppa3), a maternal factor required for the maintenance of DNA methylation in early embryos, induced global DNA hypomethylation and transformation in NIH3T3 cells. This hypomethylation was due to the binding of Stella to Np95 (also known as Uhrf1, ICBP90) and the subsequent impairment of Dnmt1 localization. In addition, enforced expression of Stella enhanced the metastatic ability of B16 melanoma cells through the induction of metastasis-related genes by inducing DNA hypomethylation of their promoter regions. Such DNA hypomethylation itself causes cellular transformation and metastatic ability. These data provide new insight into the function of global DNA hypomethylation in carcinogenesis. We used microarrays to detail the global programme of gene expression by PGC7/Stella overexpression.
2016-05-13 | GSE68837 | GEO
Project description:Stella humosa DSM 5900 genome sequencing
| PRJNA500349 | ENA
Project description:Stella vacuolata DSM 5901 = ATCC 43931 Genome sequencing
| PRJNA221071 | ENA
Project description:Genome-wide DNA demethylation is a unique feature of mammalian development and naïve pluripotent stem cells. So far, it was unclear how mammals specifically achieve global DNA hypomethylation, given the high conservation of the DNA (de-)methylation machinery among vertebrates. We found that DNA demethylation requires TET activity but mostly occurs at sites where TET proteins are not bound suggesting a rather indirect mechanism. Among the few specific genes bound and activated by TET proteins was the naïve pluripotency and germline marker Dppa3 (Pgc7, Stella), which undergoes TDG dependent demethylation. The requirement of TET proteins for genome-wide DNA demethylation could be bypassed by ectopic expression of Dppa3. We show that DPPA3 binds and displaces UHRF1 from chromatin and thereby prevents the recruitment and activation of the maintenance DNA methyltransferase DNMT1. We demonstrate that DPPA3 alone can drive global DNA demethylation when transferred to amphibians (Xenopus) and fish (medaka), both species that naturally do not have a Dppa3 gene and exhibit no post-fertilization DNA demethylation. Our results show that TET proteins are responsible for active and - indirectly also for - passive DNA demethylation; while TET proteins initiate local and gene-specific demethylation in vertebrates, the recent emergence of DPPA3 introduced a unique means of genome-wide passive demethylation in mammals and contributed to the evolution of epigenetic regulation during early mammalian development.
2020-10-12 | PXD019794 | Pride
Project description:We constructed a polycistronic lentiviral vector to overexpress 3 germ cell specific genes (Stella, Oct4 and Nanos2) in mouse embryonic fibroblast (MEFs) and evaluated the transcriptome portrait in partially reprogrammed cells.We sequenced RNA samples from bulk cell population of two biological duplicates of MEF-GFP (control) and MEF-SON (overexpressed) 21 days post infection. Differential expression analysis of 50 M pair-end read per samples showed overexpression of neurogenesis, blood vessel and proliferation related genes and downregulation of chondroitin sulphate metabolic process, nitric oxide production and innate immune response genes. Examination of whole transcriptome following concurrent overexpression of Stella, Oct4 and Nanos2 in MEFs.
2016-07-30 | E-GEOD-77351 | biostudies-arrayexpress
Project description:Aspergillus stella-maris CBS 113639 Standard Draft genome sequencing
| PRJNA333886 | ENA