Jmy, also known as Junctional Mediating and Regulating Y protein, is a multifunctional protein. It serves as a transcription co-factor involved in p53 regulation, especially in the context of DNA damage. It also has a role in cytoskeleton remodelling through actin nucleation, which is associated with processes like cell motility and vesicular trafficking. Understanding Jmy is crucial as it impacts various biological processes and disease-related pathways [1,3].

In mouse models, loss-of-function studies have provided valuable insights. In Sertoli cells, loss of Sertoli cell-specific Jmy function induced male subfertility. These mice had impaired blood-tissue barrier (BTB) integrity, spermatid adhesion issues, high sperm structural deformity, reduced sperm count, and poor sperm motility. This shows Jmy's role in spermatogenesis through regulating actin filament organization and endocytic vesicle trafficking in Sertoli cells [2]. In mouse oocytes, depletion of Jmy by RNAi led to symmetric division, failure of spindle migration and cytokinesis during meiotic maturation, indicating its requirement for asymmetric division and cytokinesis in oocytes [4].

In conclusion, Jmy has essential functions in DNA damage response via p53 regulation, cytoskeleton remodelling, spermatogenesis, and oocyte maturation. The use of gene knockout (KO) mouse models in these studies has been instrumental in revealing its role in male subfertility and oocyte-related processes, providing a better understanding of related biological processes and potential disease implications.