Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting [RNA-seq]
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ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE154144 | GEO | 2021/12/22
REPOSITORIES: GEO
Similar Datasets
Project description:We asked whether oocyte number could be amplified through parthenogenesis of mouse oocytes, without requiring creation of a paternal genome and a genetically unique genome. Parthenotes develop to a blastocyst-like stage, and from this parthenogenetic ESCs (pESCs) can be derived with high efficiency. Like ESCs, pESCs maintain unlimited self-renewal and pluripotency, as well as germline competence. Further, we demonstrate that their expression pattern of imprinted maternal genes resembles that observed in oocytes. pESCs can be directed to differentiate into primordial germ cell-like cells (PGCLCs) and form oocytes that produce fertile pups and reconstitute ovarian endocrine functions. The transcriptome and imprinting pattern of PGCLCs differentiated from pESCs more closely approximate those of in vivo produced embryonic PGCs, than PGCLCs produced from ESCs. Parthenogenesis offers a promising route for deriving PGCLCs and amplifying oocytes by faithfully maintaining maternal genes, without fertilization.
2021-12-22 | GSE153979 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2021-12-22 | GSE154145 | GEO
Project description:Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting
| PRJNA645194 | ENA
Project description:Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting [RRBS]
| PRJNA644638 | ENA
Project description:Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting [RNA-seq]
| PRJNA645195 | ENA
Project description:Genomic imprinting is an allele-specific gene expression system important for mammalian development and function. The molecular basis of genomic imprinting is allele-specific DNA methylation 2. While it is well known that the de novo DNA methyltransferases Dnmt3a/b are responsible for the establishment of genomic imprinting, how the methylation mark is erased during primordial germ cell (PGC) reprogramming remains a mystery. Here we report that Tet1 plays a critical role in the erasure of genomic imprinting. We show that despite their identical genotype, progenies derived from mating between Tet1-KO males and wild-type females exhibit a number of variable phenotypes including placental, fetal and postnatal growth defects, and early embryonic lethality. These defects are, at least in part, caused by the dysregulation of imprinted genes, such as Peg10 and Peg3, which exhibit aberrant hypermethylation in the paternal allele of differential methylated regions (DMRs). RNA-seq reveals extensive dysregulation of imprinted genes in the next generation due to paternal functional loss of Tet1. Genome-wide DNA methylation analysis of E13.5 PGCs and sperm derived from Tet1-KO mice reveals hypermethylation of DMRs of imprinted genes in sperm, which can be traced back to PGCs. Dynamics of methylation change in Tet1-affected sites suggested that Tet1 swipes remaining methylation including imprinted genes at late reprogramming stage. We also revealed that Tet1play a role in paternal imprinting erasure in females germline. Thus, our study establishes a critical function for Tet1 in the erasure of genomic imprinting. Gene expression analysis of E9.5 embryos
2013-12-02 | E-GEOD-49761 | biostudies-arrayexpress
Project description:We asked whether oocyte number could be amplified through parthenogenesis of mouse oocytes, without requiring creation of a paternal genome and a genetically unique genome. Parthenotes develop to a blastocyst-like stage, and from this parthenogenetic ESCs (pESCs) can be derived with high efficiency. Like ESCs, pESCs maintain unlimited self-renewal and pluripotency, as well as germline competence. Further, we demonstrate that their expression pattern of imprinted maternal genes resembles that observed in oocytes. pESCs can be directed to differentiate into primordial germ cell-like cells (PGCLCs) and form oocytes that produce fertile pups and reconstitute ovarian endocrine functions. The transcriptome and imprinting pattern of PGCLCs differentiated from pESCs more closely approximate those of in vivo produced embryonic PGCs, than PGCLCs produced from ESCs. Parthenogenesis offers a promising route for deriving PGCLCs and amplifying oocytes by faithfully maintaining maternal genes, without fertilization.
2019-11-28 | GSE141103 | GEO
Project description:We asked whether oocyte number could be amplified through parthenogenesis of mouse oocytes, without requiring creation of a paternal genome and a genetically unique genome. Parthenotes develop to a blastocyst-like stage, and from this parthenogenetic ESCs (pESCs) can be derived with high efficiency. Like ESCs, pESCs maintain unlimited self-renewal and pluripotency, as well as germline competence. Further, we demonstrate that their expression pattern of imprinted maternal genes resembles that observed in oocytes. pESCs can be directed to differentiate into primordial germ cell-like cells (PGCLCs) and form oocytes that produce fertile pups and reconstitute ovarian endocrine functions. The transcriptome and imprinting pattern of PGCLCs differentiated from pESCs more closely approximate those of in vivo produced embryonic PGCs, than PGCLCs produced from ESCs. Parthenogenesis offers a promising route for deriving PGCLCs and amplifying oocytes by faithfully maintaining maternal genes, without fertilization.
2023-10-26 | GSE141172 | GEO
Project description:Faithful maintenance of genomic imprinting is essential for mammalian development. While germline DNA methylation-dependent (canonical) imprinting is relatively stable during development, the recently discovered oocyte-derived H3K27me3-mediated noncanonical imprinting is mostly transient in early embryos with only a few genes maintain imprinted expression in the extraembryonic lineage. How these few noncanonical imprinted genes maintain their extraembryonic-specific imprinting is unknown. Here we report that maintenance of extraembryonic-specific noncanonical imprinting requires maternal allele-specific de novo DNA methylation (secondary differentially methylation regions; DMRs) at implantation. The secondary DMRs are located at the gene promoters with paternal allele-specific H3K4me3 preformed during preimplantation development. Importantly, genetic ablation of Eed and DNA methyltransferases revealed that both maternal H3K27me3 and zygotic Dnmt3a/3b are required for establishing secondary DMRs and for maintaining noncanonical imprinting. Thus, our study not only reveals the mechanism underlying maintenance of noncanonical imprinting, but also sheds light on how histone modifications in oocytes and preimplantation embryos may shape the secondary DMRs in post-implantation embryos.
2019-12-26 | GSE130115 | GEO
Project description:Genomic imprinting confers parent-of-origin-specific gene expression, thus non-equivalent and complementary function of parental genomes. As a consequence, genomic imprinting poses an epigenetic barrier to parthenogenesis in sexual organisms. We report aberrant imprinting in Boechera, a genus in which apomicts evolved from sexuals multiple times. Maternal activation of a MADS-box gene, a homolog of which is imprinted and paternally expressed in the sexual relative Arabidopsis, is accompanied by locus-specific DNA methylation changes in apomicts where parental imprinting seems to be relaxed.
| S-EPMC6045609 | biostudies-literature