Stella prevents excessive de novo DNA methylation during mouse oogenesis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA312776 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3181060.fastq.gz | Fastqsanger.gz | |||
| SRR3181080.fastq.gz | Fastqsanger.gz | |||
| SRR3181061.fastq.gz | Fastqsanger.gz | |||
| SRR3181071.fastq.gz | Fastqsanger.gz | |||
| SRR3181081.fastq.gz | Fastqsanger.gz |
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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 -/-.
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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: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.
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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.
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Project description:UHRF1 maintains DNA methylation by recruiting DNA methyltransferases (DNMT’s) to chromatin. These dynamics are well defined for mouse STELLA (mSTELLA) but poorly characterized for human STELLA (hSTELLA). Herein, we demonstrate that hSTELLA is defective, while mSTELLA is fully proficient in associating with UHRF1 and inhibiting the abnormal DNA methylation and oncogenic functions of UHRF1 in human cancer cells. We illustrate, in structural studies a region of low sequence homology between the above STELLA orthologs, allows mSTELLA but not hSTELLA to bind tightly to the essential histone binding domains of UHRF1, thus mediating their above functional differences. The ortholog-specific binding modes of STELLA proteins with UHRF1 prompt us to explore a rationale for designing UHRF1 inhibitors for cancer therapy. For this, we use a lipid nanoparticle (LNP)-mediated mRNA delivery approach demonstrating the short mSTELLA, but not hSTELLA regions are required to reverse cancer-specific DNA methylation abnormalities and impair CRC tumor growth.
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