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Loss of Nectin-2 at Sertoli-Spermatid: INTRODUCTION(4)

We have very recently described the presence of a novel, heterotypic adhesion system at Sertoli-spermatid junctions, which is maintained by nectin-2 expressed on Sertoli cells and nectin-3 expressed on elongated spermatid heads. In the course of these studies, we have made use of a nec-tin-2-deficient mouse line (nectin-2LacZ/LacZ). We observed that the loss of nectin-2 leads to severely deformed spermatozoa, which likely is the result of improperly formed Sertoli-spermatid junctions. Moreover, a direct colocalization between nectin-2/nectin-3 and actin bundles was observed that was lost in nectin-2LacZ/LacZ testis.

Here, we describe in detail the generation and characterization of nectin-2LacZ/LacZ mice and analyze the resulting male-specific infertility phenotype. We have confirmed that nectin-2 and nectin-3 are strongly expressed at Sertoli-sper-matid junctions and that nectin-3 localization at this junction is disturbed in the absence of nectin-2, which presumably leads to the aberrant head and midpiece morphology of nectin-2LacZ/LacZ spermatozoa. Furthermore, we report here that espin, an actin-bundling protein specifically expressed at Sertoli cell ectoplasmic specializations, is virtually absent at Sertoli-spermatid junctions in nectin-2LacZ/LacZ testis. Through expression analysis of a LacZ knockin gene within the defunct mouse nectin-2 gene in nectin-2LacZ/LacZ mice, we provide additional evidence that nectin-2 present at Sertoli-spermatid junctions is contributed by the Sertoli cell.

While this work was in progress, Bouchard et al. described the generation of a nectin-2 knockout mouse using a strategy different from the one described here. The similarity and differences between the two systems will be discussed.