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Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting [RRBS]

ABSTRACT: Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting [RRBS]

PROVIDER: PRJNA644638 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR12168820_1.fastq.gz	Fastqsanger.gz
	SRR12168820_2.fastq.gz	Fastqsanger.gz
	SRR12168821_1.fastq.gz	Fastqsanger.gz
	SRR12168821_2.fastq.gz	Fastqsanger.gz
	SRR12168822_1.fastq.gz	Fastqsanger.gz

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Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting [RRBS]

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

Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting

Project description:Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting

| PRJNA645194 | ENA

Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting [RNA-seq]

Project description:Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting [RNA-seq]

| PRJNA645195 | ENA

Amplification of Oocytes through Parthenogenesis [RRBS]

2023-10-26 | GSE141172 | GEO

Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting [RNA-seq]

Project description:We perform E9.5 PGC RNA-seq for indentify the germ cell marker genes and imprinting genes expression.

2021-12-22 | GSE154144 | GEO

Amplification of Oocytes through Parthenogenesis

2019-11-28 | GSE141103 | GEO

Amplification of Germ Cells through Parthenogenesis Faithfully Maintain Genomic Imprinting

Project description:This SuperSeries is composed of the SubSeries listed below.

2021-12-22 | GSE154145 | GEO

Amplification of Oocytes through Parthenogenesis

Project description:Amplification of Oocytes through Parthenogenesis

| PRJNA592123 | ENA

RRBS of hESCs harboring imprinting-related genetic perturbations

Project description:RRBS of hESCs harboring imprinting-related genetic perturbations

| PRJEB48076 | ENA

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

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. Genome-wide DNA methylation analysis of E13.5 PGCs from control and Tet1-KO mice

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

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