Spermatogenesis in XOSxr, XXSxr, and XYSxr mice

The focus of this study was the investigation of the role of the Y chromosome in spermatogenesis by the analysis of morphological and biochemical aspects of spermatogenesis in XXSxr males, in XYSxr males, and, in particular, in XOSxr males, which lack a significant portion of the Y chromosome, but have a single X chromosome, as do normal XY mice. The results suggest that a gene controlling Sertoli cell differentiation is encoded within the Sxr segment. In addition, it was found that meiotic cells, as well as post-meiotic cells, were significantly reduced in number in these mice. The reductions in spermatocyte and early spermatid numbers are probably due to improper sex chromsome pairing and/or inactivation. The dramatic reduction in spermatid number may also be due to a decrease in the communication between spermiogenic cells and Sertoli cells. All spermatocytespecific and spermatid-specific structures, and at least two spermatid-specific proteins (basic nuclear proteins and LDH-C₄), were assembled in the correct temporal and spatial pattern in XOSxr mice. These observations suggest that these structures are not encoded on the large portion of the Y chromosome that is missing in XOSxr mice. Morphological abnormalities observed in pachytene spermatocytes and in spermatids were not unique to mice carrying the Sxr mutation and may reflect a disturbed testicular environment rather than the lack of Y-encoded products. Studies assessing sperm function demonstrated that sperm from XOSxr mice could bind to the zonae pellucidae of mouse eggs, although they did so at a reduced efficiency. These data 111 indicate that the receptors necessary for sperm binding to the zona pellucidae are present and, therefore, the genes which encode them must not be part of the Y chromosome missing in XOSxr mice.