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Spermatogenesis is a reproductive system process that produces sperm. Ubiquitin specific peptidase 26 (USP26) is an X chromosome-linked deubiquitinase that is specifically expressed in the testes. It has long been controversial whether  USP26  variants are associated with human male infertility. Thus, in the present study, we introduced a mutation into the  Usp26  gene in mice and found that  Usp26  mutant males backcrossed to a DBA/2 background, but not a C57BL/6 background, were sterile or subfertile and had atrophic testes. These findings indicate that the effects of the  Usp26  mutation on male reproductive capacity were influenced by genetic background. Sperm in the cauda epididymis of  Usp26  mutant mice backcrossed to a DBA/2 background were decreased in number and showed a malformed head morphology compared to those of wild-type mice. Additionally, histological examinations of the testes revealed that the number of round and elongated spermatids were dramatically reduced in  Usp26  mutant mice. The mutant mice exhibited unsynapsed chromosomes in pachynema and defective chiasma formation in diplonema, which presumably resulted in apoptosis of metaphase spermatocytes and subsequent decrease of spermatids. Taken together, these results indicate that the deficiencies in fertility and spermatogenesis caused by mutation of  Usp26  were dependent on genetic background.

Usp26 mutation in mice leads to defective spermatogenesis depending on genetic background