Cathepsin B Regulates Ovarian Reserve Quality and Quantity via Mitophagy by Modulating IGF1R Turnover.

The quality and quantity of the ovarian reserve are meticulously regulated through various cell death pathways to guarantee the availability of high-quality oocytes for fertilization. While apoptosis is recognized for contributing to maintaining ovarian reserve, the involvement of other cell death pathways remains unclear. Employing chemical genetics and proteomics, this study reveals the crucial involvement of Cathepsin B in maintaining the ovarian reserve.

α-tocopherol deficiency in follicular ovarian cyst (FOCs) follicular fluid (FF) elevates oxidative stress and impairs oocyte maturation.

Follicular ovarian cysts (FOCs) are prevalent reproductive disorders in both humans and animals, especially in livestock, where they cause economic losses by reducing fertility and productivity. FOCs are marked by a dominant follicle that fails to ovulate, disrupting the estrous cycle and reproductive efficiency. Previous studies indicate that the follicular fluid (FF) in cystic ovaries shows oxidative imbalance, affecting oocyte quality by altering glutathione peroxidase (GPX1) and selenium pathways.

Glutathione peroxidase (GPX1) - Selenocysteine metabolism preserves the follicular fluid's (FF) redox homeostasis via IGF-1- NMD cascade in follicular ovarian cysts (FOCs).

Follicular ovarian cysts (FOCs) are characterized by follicles in the ovaries that are >20 mm in diameter and persist for >10 days without the corpus luteum, leading to anovulation, dysregulation of folliculogenesis and subfertility in humans and livestock species. Despite their clinical significance, the precise impact of FOCs on oocyte reserve, maturation, and quality still needs to be explored. While FOCs are observed in both human and livestock populations, they are notably prevalent in livestock species.

Diminished NAD+ levels and activation of retrotransposons promote postovulatory aged oocyte (POAO) death.

Death is the fate of postovulatory aged or unfertilized oocytes (POAO) in many animals. However, precise molecular mechanisms are yet to be discovered. Here, we demonstrate that increased amounts of reactive oxygen species (ROS), calcium ion (Ca+2) channels, and retrotransposon activity induce apoptosis, which in turn causes POAO death.

Balanced spatiotemporal arrangements of histone H3 and H4 posttranslational modifications are necessary for meiotic prophase I chromosome organization.

Dynamic nuclear architecture and chromatin organizations are the key features of the mid-prophase I in mammalian meiosis. The chromatin undergoes major changes, including meiosis-specific spatiotemporal arrangements and remodeling, the establishment of chromatin loop-axis structure, pairing, and crossing over between homologous chromosomes, any deficiencies in these events may induce genome instability, subsequently leading to failure to produce gametes and infertility. Despite the significance of chromatin structure, little is known about the location of chromatin marks and the necessity of their balance during meiosis prophase I.

Local DNA synthesis is critical for DNA repair during oocyte maturation.

Mammalian oocytes can be very long-lived cells and thereby are very likely to encounter DNA damage during their lifetime. Defective DNA repair may result in oocytes that are developmentally incompetent or give rise to progeny with congenital disorders. During oocyte maturation, damaged DNA is repaired primarily by non-homologous end joining (NHEJ) or homologous recombination (HR).