is not essential for spermatogenesis and male fertility in mice.

Thousands of genes are expressed in the testis of mice. However, the details about their roles during spermatogenesis have not been well-clarified for most genes. The purpose of this study was to examine the effect of deficiency on mouse spermatogenesis and male fertility. -knockout (KO) mice were generated using CRISPR/Cas9 technology on C57BL/6J background. We found no obvious differences between -KO and -WT mice in fertility tests, testicular weight, sperm concentrations, or morphology. Histological analysis found that -KO mouse testes had normal germ cell types and mature sperm. These findings indicated that was dispensable for male fertility in mice. Our results may save time and resources by allowing other researchers to focus on genes that are more meaningful for fertility studies. We also found that mRNAs of two family members ( and ) were expressed on higher mean levels in -KO total mouse testes, compared to -WT mice. This effect was not found in mouse GC-1 and GC-2 germ cell lines with the gene transiently knocked down. This result may indicate that a gene compensation phenomenon was present in the testes of -KO mice.