While this work was ongoing, Bouchard et al. generated a similar nectin-2 knockout mouse line. In theirs as well as in our experiments, only one founder line was obtained. Therefore, our mouse nectin-2LacZ/LacZ line serves as an important validation of the infertility phenotype described earlier. A significant difference in our line is the presence of an in-frame fusion of a LacZ reporter into the nectin-2 gene that provided us with an additional tool for assessing the activity of the nectin-2 promoter by LacZ detection in nectin-2LacZ/LacZ mouse tissue.
Although male infertility in nectin-2-deficient mice results from aberrant progression of spermiogenesis leading to aberrantly shaped sperm, at the functional level this infertility phenotype is only manifested later, at the time of sperm-oocyte interaction and penetration (Figs. 4 and 5 and Table 2). Nectin-2 itself is absent on mature mouse spermatozoa; therefore, it cannot play a direct role in gamete interaction. Thus, the question arises of how the distortion of molecular structure at the sperm surface of nectin-2bacZ/LacZ spermatozoa causes the failure in fertilization. Gamete interactions leading to successful fertilization are dependent on a number of discrete steps involving specific receptors and their ligands, both at the level of sperm interaction with the zona pellucida and, distinctly, with the oolemma. pictures of asthma inhalers