Establishing and maintaining the complex adhesions of the testes: a role for the omega‐3 DHA

Abstract

Spermatid maturation and retention in the testis depend on the establishment and maintenance of a cell adhesion complex formed between spermatids and Sertoli cells. Deficiency in docosahexaenoic acid (DHA) was recently shown to disrupt postmeiotic germ cell maturation and result in infertility; however a role for DHA in germ cell adhesion has yet to be defined. Here, we use Fads2−/− mice to investigate the effect of a DHA deficiency on this adhesion process. We show impaired retention of immature spermatids in the seminiferous epithelium and their abnormal appearance in the nearest distal tissue, the epididymis. With immunohistochemistry we show that an essential adhesion protein expressed in spermatids (nectin‐3), and its binding partner in Sertoli cells (nectin‐2), each fail to organize at the sites of spermatid‐Sertoli contact, whereas both proteins organize normally in other regions of these cells. Further, vesicular transport proteins golgin‐97 and VAMP4, normally redistributed to the spermatid‐Sertoli adhesion at the initiation of its assembly, failed to do so under a DHA deficiency. In conclusion, spermatid retention is impaired under DHA deficiency due to a failure of spermatid‐Sertoli adhesion construction; the selective mislocalization of nectin‐2 and nectin‐3 suggests a role for DHA in certain specialized systems of complex adhesion assembly.Grant Funding Source: Hatch project ILLU‐971–354 through the Division of Nutritional Sciences Vision 20/20 program