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Single cell RNA-seq of the Dppa3-KO mouse embryos at 4-cell stage and 8-cell stage

ABSTRACT: We found that the DNA methylation heterogeneity was largely programmed by the initial DNA methylation state in zygote by building a mathematical model. Further, to clarify the causality of transcriptional expression heterogeneity and DNA methylation heterogeneity, we disrupted DNA methylation status during mouse early embryogenesis by knocked out (KO) DNA methylation-related genes Dppa3 in gamete cells. Then we performed single cell RNA-seq on each cell of the KO embryos in 4-cell stage and 8-cell stage.

INSTRUMENT(S): HiSeq X Ten

ORGANISM(S): Mus musculus

SUBMITTER: Chengchen Zhao

PROVIDER: E-MTAB-9360 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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LINE-1 DNA methylation levels in DPPA3 KO overexpressing DPPA3 mutants

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Role of Tet1 in genomic imprinting erasure [RRBS-PGC]

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2013-12-02 | E-GEOD-49762 | biostudies-arrayexpress

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Project description:Genome-wide DNA demethylation, including the erasure of genome imprints, in primordial germ cells (PGCs), is critical as a first step for creating the totipotent epigenome in the germ line. Here, we provide evidence that contrary to the prevailing model involving active DNA demethylation, imprint erasure in mouse PGCs occurs in a manner consistent with replication-coupled passive DNA demethylation: PGCs erase imprints during their rapid proliferation with little de novo as well as maintenance DNA methylation potential and no major chromatin alterations. Our findings necessitate the re-evaluation of and provide novel insights into the mechanism of genome-wide DNA demethylation in PGCs. We performed expression analysis of primordial germ cells (PGCs) at embryonic days 10.5-13.5. Because the number of PGCs available at these stages were low, cDNAs were amplified by the method that we previously published (Kurimoto et al. 2006, NAR 34: e42 (PMID 16547197)). To include analysis of PGC gene expression at E9.5, we re-normalized the data from our E9.5 PGC samples (GSM744103, GSM744104) from our previous publication (Hayashi et al., 2011, Cell 146: 519-32 (PMD 21820164)) together with the data from this submission.

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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.

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Project description:We report a single-cell whole-genome bisulfite sequencing method (scBS-Seq) capable of accurately measuring DNA methylation at up to 36% of CpGs. We observed that ESCs grown in serum/LIF or 2i/LIF both display epigenetic heterogeneity, with M-bM-^@M-^\2i-likeM-bM-^@M-^] cells present in serum cultures. In silico integration of 12 individual MII oocytes datasetsM-BM- recapitulates the whole DNA methylome, making scBS-Seq a versatile tool to explore DNA methylation in rare cells and heterogeneous populations. scBS-Seq has been performed on mouse MII oocytes for technical validation and on mouse ESCs cultured in 2i/LIF and serum/LIF to investage epigenetic heterogeneity

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RNA-seq and RRBS of developing zebrafish larval brain and WGBS of 4 week old WT and dnmt3aa/dnmt3ab CRISPR/CAS9 KO brain

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Amplicon bisulfite sequencing of LINE-1 elements in TET catalytic mutants and DPPA3 KO ESCs rescued by doxycylin induced overexpression

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2020-10-23 | E-MTAB-9654 | biostudies-arrayexpress

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Project description:Degradation of maternal proteins by the ubiquitin-proteasome system (UPS) accompanies the maternal-to-zygotic transition. DPPA3/Stella/PGC7, encoded by a maternal effect gene, is present in the nucleus and cytoplasm of zygotes and has been associated with protecting the female pronucleus from TET3-mediated demethylation. We now report that cytoplasmic DPPA3 is partially cleaved by the ubiquitin-proteasome system and an N-terminus fragment remains in the cytoplasm where it associates with early and re-cycling endosomes. If DPPA3 is absent or if cleavage is prevented, multiple vesicles coalesce/aggregate and markers of lysosomes are decreased. Fertilized eggs develop poorly into blastocysts, which results in significantly decreased fecundity of Dppa3 R60A transgenic mice. This phenocopies aspects of Lamp1/2 knockdowns and Dppa3 KO embryos can be partially rescued in vitro by DPPA31-60 and to a lesser extent by LAMP1/2. Thus, the N-terminus of DPPA3 has a significant role in cytoplasmic vesicular trafficking in addition to its previously reported nuclear function.

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