Figure 6. Altered gene expression in Ctnnb1 FΔ testes.

(A) QPCR analyses of genes in Table S2 on purified round spermatid RNA pooled from four mice using primers in Table S3. (B) Model of β-catenin signaling cascade at the apical ES. Since MAPK signaling proteins play a role in actin restructuring [21], [22], [23], we propose that β-catenin may stabilize the actin cytoskeleton network on germ cell surfaces by activating negative regulators (Dusp26) and inhibiting positive regulators (MKK7 and MK2) of MAPK signaling. We also posit that the junction restructuring event at the apical ES is affected by β-catenin's ability to regulate factors such as Lrrn3 and Vps33a, which are implicated in recycling and degrading proteins through endocytosis [24], [25], [26]. Since β-catenin is known to play an important role in cadherin recycling at the epithelial cell surface [77], we propose that β-catenin deletion would result in altered recycling and degradation of cadherin on the germ cell surface leading to loss of Sertoli cell-germ adhesion at the apical ES. In addition to Sertoli cell-germ cell adhesion, β-catenin may also directly influence vesicle trafficking (and subsequently junction export and acrosome formation) and germ cell polarity by interacting with polarity proteins JAM-C and Cdc42. Finally, β-catenin may regulate chromatin compaction during spermatid development by affecting the expression of Dtl and Arpc5, which we and others have shown to regulate chromatin compaction of differentiating germ cells.