Abstract

Adenylate cyclase 3 (AC3) is an important component of the cyclic adenosine 3′,5′-monophosphate (cAMP) signaling pathway and converts adenosine triphosphate into cAMP. Male mice with AC3 deletion (AC3−/−) are sterile. However, the mechanical mechanism remains unclear. By TUNEL staining, we found that cell apoptosis in the testicular tissues of AC3−/− mice increased significantly compared with that in the wild-type (AC3+/+) mice. Differentially expressed genes regulated by AC3 in the testicular tissues were identified by gene chip hybridization. We observed that the expression of 693 genes was altered in the testicular tissues of AC3−/− mice, including 330 up-regulated and 363 down-regulated gene expression with fold changes higher than 2 (≥2) as the standards. Furthermore, part of these differentially expressed genes was verified by the real-time fluorescence quantification PCR and immunofluorescent staining. The expression levels of the genes related to olfactory receptors, cell apoptosis, transcriptional activity, defensive reaction, cell adhesion, cell death, and immunoreactions were significantly altered in the testicular tissues of AC3−/− mice compared with AC3+/+ mice. In addition, the corresponding Ca2+, cAMP, and cell adhesion signaling pathways, as well as the signaling pathways related to axon guidance and cell interaction, were altered significantly in the AC3−/− mice. These data would help elucidate the general understanding of the mechanisms underlying the sterility in AC3−/− male mice.

Full Text
Published version (Free)

Talk to us

Join us for a 30 min session where you can share your feedback and ask us any queries you have

Schedule a call