Samd7 is dispensable for spermatogenesis and male fertility in mice

Although many genes have been implicated in spermatogenesis, their precise relationships to male fertility remain unclear. Here, we investigated the in vivo importance of the highly conserved, testis-enriched gene Samd7 as a potential regulator of murine spermatogenesis and fertility.

Samd7^-/- mice were generated using CRISPR/Cas9. qPCR was used to assess Samd7 mRNA expression across mouse tissues. SAMD7 protein levels in testis were examined by Western blotting. Hematoxylin and eosin (H&E) staining of testis and epididymis was performed to evaluate spermatogenesis and sperm maturation. Immunofluorescence was used to characterize developmental stages of germ cells in the testis. Computer-assisted sperm analysis (CASA) was employed to measure sperm motility and related parameters.

Samd7 expression was enriched in testis beginning at postnatal week 3. Compared with wild-type (Samd7^+/+) littermates, Samd7^-/- males showed no abnormalities in sperm content, testicular morphology, or fertility. Histology confirmed intact seminiferous tubules and normal testicular architecture in both Samd7^+/+ and Samd7^-/- mice. No differences were detected in sperm morphology or motility, including swimming velocity, in Samd7^-/- mice. Testes and epididymides from Samd7^-/- animals contained the expected spectrum of germ cells-from spermatogonia to mature spermatozoa-consistent with unimpaired spermatogenesis.

These findings indicate that Samd7 is dispensable for murine spermatogenesis and male fertility under standard laboratory conditions.