Golga3, also known as Mea2, is a member of the golgin subfamily A. It is a Golgi complex-associated protein involved in protein transport, cell apoptosis, Golgi localization, and spermatogenesis [1,2,3]. It has eight phosphorylation sites, and its function may also be related to pathways like ubiquitin-dependent proteasomal degradation as it interacts with serine racemase [4]. Genetic mouse models are valuable for studying its functions.

In mouse models, Golga3 knockout (KO) male mice show infertility [2]. In Golga3(repro27) mutant mice with a nonsense mutation in Golga3, spermatogenesis initiates normally but is disrupted in late meiosis, leading to germ cell loss, abnormal spermiogenesis, and low sperm concentration and motility [2]. However, mutation of the S461 phosphorylation site in Golga3 does not affect mouse spermatogenesis [1]. Also, in a transgenic mouse where Golga3/Mea2 was disrupted, a truncated form (DeltaMea2) restored spermatogenesis in a dose-dependent manner, suggesting the importance of Golga3 for pachytene spermatocyte survival [3].

In conclusion, Golga3 is crucial for spermatogenesis as demonstrated by KO mouse models. Defects in Golga3 lead to male infertility due to disrupted spermatogenesis. These models have enhanced our understanding of the role of Golga3 in male germ cell development and may have implications for understanding human male infertility [1,2,3].