CONTROL OF THE SURFACE EXPRESSION OF UVOMORULIN AFTER ACTIVATION OF MOUSE OOCYTES

Uvomorulin (E-cadherin) is the major cell adhesion molecule responsibl e for intercellular adhesion in early mouse embryos. In contrast to ot her cell adhesion molecules, it is not detectable on the cell surface until around 6 h after fertilisation or parthenogenetic activation, at the time when pronuclear formation occurs (Clayton, L., Stinchcombe, S.V. and Johnson, M.H., Zygote 1, 333-44, 1993). In order to investiga te this developmental control of surface expression of uvomorulin, we examined the effects of inhibitors of various cellular processes on th e appearance of uvomorulin at the oocyte surface, as assessed immunocy tochemically. Inhibitors of cytoskeletal assembly (cytochalasin D and nocodazole), protein synthesis (puromycin and anisomycin), and DNA syn thesis (aphidicolin) had no effect on surface expression. Brefeldin A, which inhibits intracellular transport and secretion, did prevent sur face expression, but monensin did not. The effects of brefeldin were r eversible; following 8 h of treatment, recovery of surface expression after removal of brefeldin began within 2 h. The time-course of surfac e expression post-activation suggested a link with pronuclear formatio n. However, when pronuclear formation was advanced experimentally usin g 6-dimethylaminopurine (DMAP), concomitant advancement of surface uvo morulin was not observed. Similarly, surface expression of uvomorulin did not accompany puromycin-induced pronuclear formation in maturing m eiotic metaphase 1 (MI) oocytes in vitro. Thus, surface uvomorulin exp ression does not appear to be linked simply to pronuclear formation. P roteolytic processing of both newly synthesised and total uvomorulin t o generate mature molecule from precursor increased within 30 min to 1 h after activation, and also occurred in the continued presence of bre feldin, suggesting that uvomorulin processing appears to be controlled independently of its surface expression.