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Loss of Nectin-2 at Sertoli-Spermatid: DISCUSSION(1)

Spermatogenesis, the progression from a diploid sper-matogenic stem cell to a highly specialized, motile, flagellated, haploid cell (i.e., the spermatozoon), presents one of the most dramatic differentiation processes in biology. This metamorphosis depends on a complex relationship between the differentiating germ cell and Sertoli cells that form the seminiferous epithelium. At least two types of cell-cell junctions are critically involved in maintaining the integrity of the seminiferous epithelium. Specialized Ser-toli-Sertoli junctional complexes (basal ectoplasmic specializations) separate the basal and adluminal compartments of the seminiferous epithelium by generating the BTB. Apical ectoplasmic specializations between Sertoli cells and elongated spermatids appear to be critical for morphogenesis and translocation of maturing spermatids, and their disassembly is required for release of spermatozoa into the lumen of the tubule. review

Most morphological changes of the differentiating spermatid occur in the later stages of spermiogenesis (steps 816) as round spermatids elongate their nuclei, condense their chromatin, shed most of their cytoplasm, and extend the sperm tail. During this time, spermatogenesis in nectin-2-deficient males appears to deviate from the normal developmental program. Nectin-2 is only expressed on Sertoli cells and not on spermatids (see above). Consequently, the observed aberrant morphology of spermatozoa in nectin-2-deficient mice likely results from the absence of exterior forces exerted by the Sertoli cell onto the developing spermatid. In wt testes, these forces seem to be transmitted from the Sertoli cell to the spermatid by the nectin-2/nectin-3 adhesion unit.