Sus scrofa
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA381067 | ENA |
REPOSITORIES: ENA
Similar Datasets
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Project description:Spermidine is involved in a variety of biological processes, including DNA metabolism, autophagy and aging. Previous studies have shown that spermidine can increase the percentage of mouse oocytes developing into blastocysts after in vitro fertilization. However, none of the past studies elucidated the effects of spermidine supplementation on porcine oocyte maturation. Here, we choose appropriate dose of spermidine to be added to the maturation medium during in vitro maturation (IVM) to verify whether spermidine can actively promote the maturation of porcine oocytes. Our study provided substantial evidence that spermidine exposure promoted the porcine oocyte meiotic maturation. In addition, single-cell transcriptome analysis identified the target effectors of spermidine actions in porcine oocytes, further demonstrating that spermidine exposure enhanced mitochondrial distribution and function, leading to a reduced excessive oxidative stress-induced DNA damage and early apoptosis of porcine oocytes. These findings demonstrate that spermidine not only delays ageing and cancer treatment, but also improves the quality of germ cells, which may be less likely to suffer from sterility or infertility in humans and animals.
2024-11-30 | GSE217447 | GEO
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Project description:In vitro maturation (IVM) oocyte is a key component of assisted reproduction in pigs. Asynchronous nucleoplasmic maturation and incomplete cytoplasmic maturation is one of the key factors for impaired maturation and quality of oocytes matured in vitro. Although Single-omics techniques have been applied to the study of porcine oocyte maturation mechanisms in the past, it is difficult to address a systematic and comprehensive explanation of the complex maturation regulatory network through Single-omics data alone, and it is insufficient to account for the chain of transmission of the regulation of genetic information expression. This is the first study which determine the gene transcripts, host potential proteins interactions, and key functional metabolites involved in the maturation mechanism of porcine oocytes. We found that among 2624 and 124 differentially expressed genes and proteins respectively, genes DNMT1, HENMT1, H1FOO, GDF9, NUP214, CAST and GSTM3 were differentially coexisted at both levels，these differentially expressed genes are closely associated with 13 differentially expressed metabolites.In addition, the genes DNMT1 , HENMT1, H1FOO, GDF9, NUP214, CAST and GSTM3 were differentially expressed at both transcript and protein levels. To address further functional analysis, we conducted GO and KEGG analysis at mRNAs and metabolites level to outcome the involvement of multiple epigenetic regulatory mechanisms affecting nuclear and cytoplasmic maturation of porcine oocytes. Thus, we systematically illustrated how epigenetic modifications affect nuclear and cytoplasmic maturation of porcine oocytes from the dimension of the transmission chain of genetic information expression regulation. Specifically, it includes: 1) .The increase in DNA methylation level and the decrease in histone acetylation level lead to the reduction of chromatin accessibility, thereby triggering global transcriptional silencing. 2).A large number of mRNAs that have been transcribed in the nucleus need to undergo complex modifications before they can be recognized by the nuclear pore complex (NPC) and transported to the cytoplasm. 3). The mRNAs transported to the cytoplasm are selectively translated activated according to the requirements of the cell maturation process. This spatiotemporal heterogeneity of translation activation is strictly regulated by post-transcriptional modifications. 4 ). Post-translational modifications regulate the active sialic acid metabolism to prepare for the fertilization process; the macro and micro changes in glutathione metabolism and mitochondrial metabolism aim to meet the dynamic energy requirements of the cell and regulate intracellular redox homeostasis to reduce oxidative damage.
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