Loss of myosin VI expression affects acrosome/acroplaxome complex morphology during mouse spermiogenesis. Issue 3 (15th May 2020)

• Record Type: Journal Article
• Authors: Zakrzewski, Przemysław; Rędowicz, Maria Jolanta; Buss, Folma; Lenartowska, Marta
• Is Part Of: Biology of reproduction. Volume 103:Issue 3(2020)
• Page Start: 521
• Page End: 533
• Publication Date: 2020-05-15
• Subjects: acrosome/cap -- acroplaxome -- actin cytoskeleton -- Golgi complex -- myosin VI -- Snell's waltzer mice; Reproduction -- Periodicals; Biology; Reproduction; Reproduction; Electronic journals; Periodicals; Periodicals; 571.805
• DOI: 10.1093/biolre/ioaa071
• Languages: English
• ISSNs: 0006-3363

Abstract

Abstract: During spermiogenesis in mammals, actin filaments and a variety of actin-binding proteins are involved in the formation and function of highly specialized testis-specific structures. Actin-based motor proteins, such as myosin Va and VIIa, play a key role in this complex process of spermatid transformation into mature sperm. We have previously demonstrated that myosin VI (MYO6) is also expressed in mouse testes. It is present in actin-rich structures important for spermatid development, including one of the earliest events in spermiogenesis—acrosome formation. Here, we demonstrate using immunofluorescence, cytochemical, and ultrastructural approaches that MYO6 is involved in maintaining the structural integrity of these specialized actin-rich structures during acrosome biogenesis in mouse. We show that MYO6 together with its binding partner TOM1/L2 is present at/around the spermatid Golgi complex and the nascent acrosome. Depletion of MYO6 in Snell's waltzer mice causes structural disruptions of the Golgi complex and affects the acrosomal granule positioning within the developing acrosome. In summary, our results suggest that MYO6 plays an anchoring role during the acrosome biogenesis mainly by tethering of different cargo/membranes to highly specialized actin-related structures. Abstract : Myosin VI is required for the maintenance of correct morphology of testis-specific actin-containing structures important for acrosome development in mouse such as the Golgi complex and the acrosome–acroplaxome complex.