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Single-cell Transcriptomes and Follicular Fluid Proteomics of Ovine Atretic Follicles Reveal the Underlying Mechanisms of Oocyte Degeneration

ABSTRACT: Single-cell Transcriptomes and Follicular Fluid Proteomics of Ovine Atretic Follicles Reveal the Underlying Mechanisms of Oocyte Degeneration

PROVIDER: PRJNA1118191 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29232803_1.fastq.gz	Fastqsanger.gz
	SRR29232803_2.fastq.gz	Fastqsanger.gz
	SRR29232804_1.fastq.gz	Fastqsanger.gz
	SRR29232804_2.fastq.gz	Fastqsanger.gz
	SRR29232805_1.fastq.gz	Fastqsanger.gz

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Project description:Background: In mammals, female fertility is determined by the outcome of follicular development (ovulation or atresia). Follicular atresia is a complex physiological process that results in the degeneration of oocytes from the ovary. However, the molecular mechanisms of oocyte degeneration and key protein markers of follicular atresia remain unclear. In this study, we explored the complex transcriptional regulatory mechanisms and protein profiles in oocytes and follicular fluid in atretic follicle stages using single-cell RNA sequencing and tandem mass tag proteomics. Results: First, through paired analysis of different follicle development stages, we identified 175 atresia-specific genes and eight candidate oocyte-secreted factors, including PKG1, YTHDF2, and MYC. Meanwhile, we also characterized unique features of the oocyte transcriptional landscape in the atretic follicle stage that displayed cell death-related transcriptional changes and mechanisms, such as autophagy (TBK1 and IRS4), necroptosis (PKR), and apoptosis (MARCKS). Moreover, we identified atresia-specific genes, namely FTH1, TF, and ACSL4, which may participate in regulation of oocyte ferroptosis in atretic follicles through a series of mechanisms including ferritinophagy, ferritin transport, and lipid metabolism. Additionally, we uncovered 333 differentially expressed proteins that may coordinate follicular atresia and revealed key pathways, such as negative regulation of angiogenesis, metabolic pathways, and transcription and mRNA splicing, that lead to oocyte degeneration. Finally, by combining transcriptome and proteomics analyses, we identified two oocyte-secreted biomarkers, PGK1 and ANGPT2, that may be associated with follicular atresia. Conclusions: In conclusion, our work provides a comprehensive characterization of oocyte degeneration in ovine atretic follicles, which provides a basis for establishing an oocyte quality evaluation system and understanding the mechanism of follicular atresia in sheep, as well as an important reference for in vitro production of embryos.

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Single-cell Transcriptomes and Follicular Fluid Proteomics of Ovine Atretic Follicles Reveal the Underlying Mechanisms of Oocyte Degeneration

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