Abstract
Though roles of β-catenin signaling during testis development have been well established, relatively little is known about its role in postnatal testicular physiology. Even less is known about its role in post-meiotic germ cell development and differentiation. Here, we report that β-catenin is highly expressed in post-meiotic germ cells and plays an important role during spermiogenesis in mice. Spermatid-specific deletion of β-catenin resulted in significantly reduced sperm count, increased germ cell apoptosis and impaired fertility. In addition, ultrastructural studies show that the loss of β-catenin in post-meiotic germ cells led to acrosomal defects, anomalous release of immature spermatids and disruption of adherens junctions between Sertoli cells and elongating spermatids (apical ectoplasmic specialization; ES). These defects are likely due to altered expression of several genes reportedly involved in Sertoli cell-germ cell adhesion and germ cell differentiation, as revealed by gene expression analysis. Taken together, our results suggest that β-catenin is an important molecular link that integrates Sertoli cell-germ cell adhesion with the signaling events essential for post-meiotic germ cell development and maturation. Since β-catenin is also highly expressed in the Sertoli cells, we propose that binding of germ cell β-catenin complex to β-catenin complex on Sertoli cell at the apical ES surface triggers a signaling cascade that regulates post-meiotic germ cell differentiation.
Highlights
The localization of b-catenin in spermatid head is similar to the expression pattern of JAM-C (Figure 1B, panels e-h), a protein highly expressed in spermatids and the loss of which causes disruption of Sertoli-spermatid adhesion resulting in impaired germ cell differentiation [10]
This cellular interaction is facilitated by adherens junctional complexes such as ectoplasmic specializations (ES), which is critical for both adhesion and signaling between Sertoli cells and between Sertoli cells and germ cells [7]
The importance of Sertoli cell-germ cell interaction is evidenced by the fact that abnormal or disrupted ES contributes to spermatid sloughing and oligospermia in pathological conditions associated with reduced fertility potential, including varicocele, hyperprolactinemia, diabetes and idiopathic oligospermia [5,30,31]
Summary
Inactivation of b-catenin in post-meiotic germ cells resulted in increased germ cell apoptosis, compromised sperm motility, acrosomal defects, abnormal chromatin compaction, and loss of Sertoli cell-germ cell adhesion at the apical ES, leading to impaired fertility. Our results suggest that bcatenin expression in spermatids regulates specific events necessary for proper differentiation and maturation of post-meiotic germ cells.
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