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Depletion of oocyte dynamin-related protein 1 shows maternal effect abnormalities in embryonic development

ABSTRACT: Depletion of oocyte dynamin-related protein 1 shows maternal effect abnormalities in embryonic development

PROVIDER: PRJNA748733 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR15209351_1.fastq.gz	Fastqsanger.gz
	SRR15209351_2.fastq.gz	Fastqsanger.gz
	SRR15209352_1.fastq.gz	Fastqsanger.gz
	SRR15209352_2.fastq.gz	Fastqsanger.gz
	SRR15209353_1.fastq.gz	Fastqsanger.gz

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Depletion of oocyte dynamin-related protein 1 shows maternal effect abnormalities in embryonic development

Project description:Eggs contain about 200,000 mitochondria that generate ATP and metabolites essential for oocyte and embryo development. In addition to this energetic role, mitochondria also integrate the cellular metabolic and transcriptional state via metabolites which regulate epigenetic modifiers. The maternal epigenome is established during oogenesis, but there is no direct evidence linking oocyte mitochondrial function to the maternal epigenome and embryo development. The DRP1 protein is required for mitochondrial fission. Here, we demonstrate a dramatic maternal effect in that DRP1-deficient oocytes fertilized by wild-type sperm exhibit a high frequency of failure in peri- and post-implantation development. This failure is associated with altered oocyte mitochondrial function, changes in the oocyte transcriptome and proteome, and a decrease in oocyte DNA methylation and H3K27me3. Transplanting the pronuclei of these fertilized oocytes to normal ooplasm fails to rescue embryonic lethality. We conclude that mitochondrial function plays a role in establishing the maternal epigenome, with serious consequences for embryo development.

2021-11-01 | GSE180579 | GEO

Depletion of oocyte dynamin-related protein 1 shows maternal-effect abnormalities in embryonic development.

Project description:Eggs contain about 200,000 mitochondria that generate adenosine triphosphate and metabolites essential for oocyte development. Mitochondria also integrate metabolism and transcription via metabolites that regulate epigenetic modifiers, but there is no direct evidence linking oocyte mitochondrial function to the maternal epigenome and subsequent embryo development. Here, we have disrupted oocyte mitochondrial function via deletion of the mitochondrial fission factor Drp1. Fission-deficient oocytes exhibit a high frequency of failure in peri- and postimplantation development. This is associated with altered mitochondrial function, changes in the oocyte transcriptome and proteome, altered subcortical maternal complex, and a decrease in oocyte DNA methylation and H3K27me3. Transplanting pronuclei of fertilized Drp1 knockout oocytes to normal ooplasm fails to rescue embryonic lethality. We conclude that mitochondrial function plays a role in establishing the maternal epigenome, with serious consequences for embryo development.

| S-EPMC9200162 | biostudies-literature

Granulosa cell mevalonate pathway abnormalities contribute to oocyte meiotic defects and aneuploidy [RNA-seq mouse oocyte]

Project description:Granulosa cell mevalonate pathway abnormalities contribute to oocyte meiotic defects and aneuploidy [RNA-seq mouse oocyte]

| PRJNA857823 | ENA

Granulosa cell mevalonate pathway abnormalities contribute to oocyte meiotic defects and aneuploidy

Project description:Granulosa cell mevalonate pathway abnormalities contribute to oocyte meiotic defects and aneuploidy

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Histone variant H3.3 is an essential maternal factor for oocyte reprogramming

Project description:Mature oocyte cytoplasm can reprogram somatic cell nuclei to the pluripotent state through a series of sequential events including protein exchange between the donor nucleus and ooplasm, chromatin remodeling, and pluripotency gene reactivation. Maternal factors that are responsible for this reprogramming process remain largely unidentified. Here, we demonstrate that knockdown of histone variant H3.3 in mouse oocytes results in compromised reprogramming and down-regulation of key pluripotency genes; and this compromised reprogramming both for developmental potentials and transcription of pluripotency genes can be rescued by injecting exogenous H3.3 mRNA, but not H3.2 mRNA into oocytes in somatic cell nuclear transfer (SCNT) embryos. We show that maternal H3.3, and not H3.3 in the donor nucleus, is essential for successful reprogramming of somatic cell nucleus into the pluripotent state. Furthermore, H3.3 is involved in this reprogramming process by remodeling the donor nuclear chromatin through replacement of donor nucleus-derived H3 with de novo synthesized maternal H3.3 protein. Our study shows that H3.3 is a crucial maternal factor for oocyte reprogramming and provides a practical model to directly dissect the oocyte for its reprogramming capacity. Transcriptome sequencing of 4-cell NT embryos, Luciferase 4-cell SCNT embryos, 4-cell NT embryos_H3.3KD, 4-cell NT embryos_H3.3KD+H3.3mRNA, H3.3 KD + H3.2 mRNA SCNT embryos

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Histone variant H3.3 is an essential maternal factor for oocyte reprogramming

2014-06-02 | GSE56762 | GEO

Maternal ELL3 loss-of-function leads to oocyte aneuploidy and early miscarriage

Project description:Up to one-tenth of women experience miscarriage in their lifetime. Embryonic aneuploidy is a leading cause of infertility, miscarrage and congenital defects. Here, we identify loss-of-function variants of ELL3, a gene encoding a transcription elongation factor, from couples experienced consecutive early spontaneous miscarriages due to embryonic aneuploidy. Maternal ELL3 knockout leads to oocyte aneuploidy. Furthermore, we found that ELL3 localizes to the spindle during meiosis, and that ELL3 depletion in both mouse and human oocytes increases the incidence of meiotic spindle abnormality. Biochemically, ELL3 competes with TPX2 to interact with the microtubule motor KIF11, promoting its ATP utilization. Live imaging analysis shows that ELL3 is essential for promoting spindle elongation rate and driving chromosome movement. Our findings demonstrate that ELL3 loss-of-function variations could lead to oocyte aneuploidy and early miscarriage.

2024-10-30 | GSE268181 | GEO

Granulosa cell mevalonate pathway abnormalities contribute to oocyte meiotic defects and aneuploidy [Hi-C]

Project description:Granulosa cell mevalonate pathway abnormalities contribute to oocyte meiotic defects and aneuploidy [Hi-C]

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Granulosa cell mevalonate pathway abnormalities contribute to oocyte meiotic defects and aneuploidy [RNA-seq mouse oocyte]

Project description:The mechanisms of oocyte meiotic defects and low competence during ovarian aging remains elusive for decades. Using Hi-C (genome-wide chromatin conformation capture) and Smart RNA-seq of oocytes from 6- weeks or 10- months aged ovaries, the abnormal loose chromatin structures and disturbing expression of meiosis associated genes at metaphase I phase were disclosed. Furthermore, the transcriptomic landscape of granulosa cells (GCs) surrounding oocytes from young and aged ovaries reveled that oocyte meiotic maturation was accompanied with a robust increased expression of genes involved with the mevalonate (MVA) pathway in GCs from young ovaries but these genes expression was not upregulated to counterpart level in GCs from aged ovaries.The inhibitor of MVA pathway of GCs, Statins significantly decreased polar body extrusion rate and increased the rate of irregularly assembled spindles and misaligned chromosomes remarkably in oocytes of culumus-oocyte complex (COCs) from young ovaries . Correspondingly, the activitor of MVA pathway of GCs, Geranylgeraniol ameliorated ovarian reserve and reduced meiotic defects in oocytes of COCs from aged ovaries. Mechanistically, MVA pathway activation in GCs culminated oocyte meiotic maturation by upregulating EGF signaling via LH receptor on GCs surrounding oocytes. Together, MVA pathway is a promising therapeutic target for prompting quality of oocytes from aged ovaries.

2023-02-26 | GSE175835 | GEO

The effect of ionomycin-induced oocyte activation on multiple morphological abnormalities of the sperm flagella

Project description:The effect of ionomycin-induced oocyte activation on multiple morphological abnormalities of the sperm flagella

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