Successful fertilization requires spermatozoa to be both mechanically stable and responsive to extracellular signals, a capacity conferred by specialized cytoskeletal proteins. In mammalian spermatozoa, tektins (e.g., Tektin1–5) are filamentous structural proteins predominantly localized to the flagellum, where they stabilize the axoneme and support the motility and functional competence of the spermatozoa essential for fertilization. Given the dynamic redistribution of certain isoforms (e.g., Tektin1–3) to the sperm head during capacitation, hyperactivation, and the acrosome reaction, the molecular mechanisms through which tektins coordinate structural integrity with signaling events remain unclear. Owing to advancements in genetic tools, high-throughput sequencing, and structural biology, significant progress has been made in the past decade in elucidating the roles of tektins in spermiogenesis and fertilization. In this review, we discuss functional evidence from animal models and human genetic studies, summarize the current knowledge linking tektin deficiency or mutation to impaired sperm motility and male fertility, and highlight the potential of these genes as biomarkers and therapeutic targets in precision andrology.

Keywords: flagellar morphogenesis; male fertility; microtubule inner protein; sperm motility; sperm signaling network; tektin family