Cell adhesion and gap junction formation in the early mouse embryo are induced prematurely by 6-DMAP in the absence of E-cadherin phosphorylation.

Compaction of the mouse embryo, which takes place at the 8-cell stage, is dependent upon the adhesion molecule E-cadherin (uvomurulin), but does not require protein synthesis, suggesting that post-translational modification(s) is (are) implicated in the setting up of this phenomenon. The demonstration recently that E-cadherin is phosphorylated at the 8-cell stage just before compaction supports this theory. In this work we used 6-dimethylaminopurine, a serine-threonine kinase inhibitor, to investigate the role of protein phosphorylation in compaction of mouse embryos. 6-dimethylaminopurine is able to induce cell flattening and gap junction formation prematurely at the 4-cell stage; however, it does not induce cell surface polarization, as occurs during normal compaction. 6-dimethylaminopurine-induced premature flattening is inhibited when the embryos are cultured in the presence of an anti-E-cadherin antibody or without extra-cellular Ca2+, demonstrating that this process requires functional E-cadherin; whereas cell flattening and gap junction formation take place in the absence of E-cadherin phosphorylation, suggesting that its phosphorylation is not required normally for these events. The relationship between E-cadherin-mediated cell flattening and gap junction formation during compaction is discussed.