Arrdc5, an α-arrestin molecule, is crucial for mammalian spermatogenesis. Arrestin molecules are known to modulate cellular signaling and ubiquitination, suggesting Arrdc5 may function in related pathways [1]. Its expression is conserved and testis-enriched across multiple mammalian species, including mice, pigs, cattle, and humans [1].

In gene knockout studies, Arrdc5-deficient male mice are sterile due to low numbers of immotile and malformed sperm. Spermiogenesis, the final phase of spermatogenesis, is defective in these mice. Epididymal sperm also cannot capacitate and fertilize oocytes [1]. Another study shows that Arrdc5 knockout mice have male infertility with a high bent-head rate and reduced sperm motility, caused by its effect on NDC1 and SUN5, which are related to the sperm head-tail coupling apparatus [2].

In conclusion, Arrdc5 is an essential regulator of mammalian spermatogenesis, as revealed by KO mouse models. These models have demonstrated its role in ensuring normal sperm morphogenesis, motility, and capacitation, highlighting its significance in male fertility-related research [1,2].

References:

1. Giassetti, Mariana I, Miao, Deqiang, Law, Nathan C, Bernhardt, Miranda L, Oatley, Jon M. 2023. ARRDC5 expression is conserved in mammalian testes and required for normal sperm morphogenesis. In Nature communications, 14, 2111. doi:10.1038/s41467-023-37735-y. https://pubmed.ncbi.nlm.nih.gov/37069147/

2. Liu, Ruyi, Qu, Ronggui, Li, Qun, Zhang, Zhihua, Sang, Qing. 2023. ARRDC5 deficiency impairs spermatogenesis by affecting SUN5 and NDC1. In Development (Cambridge, England), 150, . doi:10.1242/dev.201959. https://pubmed.ncbi.nlm.nih.gov/37997706/