Single cell transcriptome analysis of human oocyte aging
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA648927 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR12330954_1.fastq.gz | Fastqsanger.gz | |||
| SRR12330954_2.fastq.gz | Fastqsanger.gz | |||
| SRR12330955_1.fastq.gz | Fastqsanger.gz | |||
| SRR12330955_2.fastq.gz | Fastqsanger.gz | |||
| SRR12330956_1.fastq.gz | Fastqsanger.gz |
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Project description:To investigate the effects of women age on oocyte developmental competency, we used single-cell RNA sequencing to detect global gene transcriptome and identify key genes affected by advanced age in human mature oocytes.
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Project description:Chromosome segregation errors in oocytes lead to the production of aneuploid eggs, which are the leading cause of pregnancy loss and of several congenital diseases such as Down syndrome. The frequency of chromosome segregation errors in oocytes increases with maternal age, especially at a late stage of reproductive life. How aging at various life stages affects oocytes differently remains poorly understood. In this study, we describe aging-associated changes in the transcriptome profile of mouse oocytes throughout reproductive life. Our single-oocyte comprehensive RNA sequencing using RamDA-seq revealed that oocytes undergo transcriptome changes at a late reproductive stage, whereas their surrounding cumulus cells exhibit transcriptome changes at an earlier stage. Calorie restriction, a paradigm that reportedly prevents aging-associated egg aneuploidy, promotes a transcriptome shift in oocytes with the up-regulation of genes involved in chromosome segregation. This shift is accompanied by the improved maintenance of chromosomal cohesin, the loss of which is a hallmark of oocyte aging and causes chromosome segregation errors. These findings have implications for understanding how oocytes undergo aging-associated functional decline throughout their reproductive life in a context-dependent manner.
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Project description:Single-cell transcriptome analysis of aging brain
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Project description:Oocyte ageing is a key bottleneck and intractable challenge for in vitro fertilization treatment of aged female patients. The underlying molecular mechanisms of human oocyte ageing remain to be elucidated. Hence, this study aims to investigate the key genes and relevant biological signalling pathways involved in human oocyte ageing. We isolated mRNA for single-cell RNA sequencing from MII human oocytes donated by patients undergoing intracytoplasmic sperm injection. Nine RNA-seq datasets were analyzed, which included 6 older patients(average 42.67±2.25 years) and 3 younger patients (average 25.67±2.08 years). 481 differentially expressed genes (DEGs) were identified, including 322 upregulated genes enriched in transcription, ubiquitination, epigenetic regulation, and cellular processes, and 159 downregulated genes enriched in ubiquitination, cell cycle, signalling pathway, and DNA repair. The STRING database was used to analyse protein-protein interactions, and the Cytoscape software was used to identify hub genes. From these DEGs, 17 hub genes were identified including 12 upregulated genes (UBE2C, UBC, CDC34, UBR1, KIF11, ASF1B, PRC1, ESPL1, GTSE1, EXO1, UBA1, KIF4A) and 5 downregulated genes (UBA52, UBE2V2, SKP1, CCNB1, MAD2L1). The significant key biological processes that are associated with these hub genes include ubiquitin-mediated proteolysis, ubiquitination-related pathways, oocyte meiosis, and cell cycle. Among these, UBE2C may play a crucial role in human oocyte ageing.
| S-EPMC8256362 | biostudies-literature
Project description:To find genes in C. elegans oocytes associated with reproductive aging. Five replicates comparing RNA from oocyte samples collected from day 3 fem-1(hc17) animals with RNA from oocyte samples collected from day 8 fem-1(hc17) animals. Three out of five are dye-flipped.
2010-09-01 | E-GEOD-23447 | biostudies-arrayexpress
Project description:Background Aging is characterized by the gradual loss of physiological integrity, resulting in impaired function and easier death. This deterioration is a major risk factor for major human pathological diseases, including cancer, diabetes, cardiovascular disease and neurodegenerative diseases. It is very important to find biomarkers that can prevent aging. Methods Q-Exactive-MS was used for proteomic detection of young and senescence fibroblast. The key senescence-related molecules (SRMs) were identified by integrating transcriptome and proteomics from aging tissue/cells, and the correlation between these differentially expressed genes and well-known aging-related pathways. Next, we validated the expression of these molecules using qPCR, and explored the correlation between them and immune infiltrating cells. Finally, the enriched pathways of the genes significantly related to the four differential genes were identified using the single cell transcriptome. Results we first combined proteomics and transcriptome to identified four SRMs. Data sets including GSE63577, GSE64553, GSE18876, GSE85358 and qPCR confirmed that ETF1, PLBD2, ASAH1, and MOXD1 were identified as SRMs. Then the correlation between SRMs and aging-related pathways was excavated and verified. Next, we verified the expression of SRMs at the tissue level and qPCR, and explored the correlation between them and immune infiltrating cells. Finally, at the single-cell transcriptome level, we verified their expression and explored the possible pathway by which they lead to aging. Briefly, ETF1 may affect the changes of inflammatory factors such as IL-17, IL-6, and NFKB1 by indirectly regulating the enrichment and differentiation of immune cells. MOXD1 may regulate senescence by affecting the WNT pathway and changing the cell cycle. ASAH1 may affect development and regulate the phenotype of aging by affecting cell cycle-related genes. Conclusion In general, based on the analysis of proteomics and transcriptome, we identified four SRMs that may affect aging and speculated their possible mechanisms, which provides a new target for preventing aging, especially skin aging.
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2010-09-01 | E-GEOD-23446 | biostudies-arrayexpress
Project description:Here we asked if oocyte proteomes are representative of the transcriptomes, how the abundance of specific genes’ mRNA and protein responds to maternal aging, and if oocyte aging presents the features characteristic of somatic aging. To address these questions on the proteomic level, we employed stable isotope labeling of amino acids in cell culture (SILAC; Geiger et al. 2011) as the method of choice, and performed a SILAC screen of mouse metaphase II (MII) oocytes superovulated at 3, 8+-1 and 58+-10 weeks of maternal age, which correspond to pre-puberty, mature age and climacterium, respectively. We used heavy F9 embryonic carcinoma (EC) cells as internal or "Spike-in" standard for the quantification of oocytes proteins because in contrast to the oocytes they can easily be cultured feeder-free, have stem cell properties and should harbor the majority of all oocyte proteins (although with different relative abundances). The SILAC screen was conducted in parallel with conventional microarray analysis to compare the concordance of protein and transcript levels in these oocytes. Associated microarray data have been deposited to NCBI GEO with accession number GSE42959.
2016-10-14 | PXD000512 | Pride
Project description:Single-cell transcriptome analysis of aging bone marrow
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