SELECTIVE DISRUPTION OF E-CADHERIN FUNCTION IN EARLY XENOPUS-EMBRYOS BY A DOMINANT-NEGATIVE MUTANT

E-cadherin function was disrupted in vivo in developing Xenopus laevis embryos through the expression of a mutant E-cadherin protein lacking its cytoplasmic tail. This truncated form of E-cadherin was designed to act as a dominant negative mutant by competing with the extracellul ar interactions of wild-type endogenous E-cadherin. Expression of trun cated E-cadherin in the early embryo causes lesions to develop in the ectoderm during gastrulation. In contrast, expression of a similarly t runcated N-cadherin protein failed to cause the lesions. The ectoderma l defect caused by the truncated E-cadherin is rescued by overexpressi on of wild-type E-cadherin, by co-injection of full-length E-cadherin RNA along with the RNA for the truncated form. Overexpression of full- length C-cadherin, however, is unable to compensate for the disruption of E-cadherin function and can actually cause similar ectodermal lesi ons when injected alone, suggesting that there is a specific requireme nt for E-cadherin. Therefore, E-cadherin seems to be specifically requ ired for maintaining the integrity of theectoderm during epiboly in th e gastrulating Xenopus embryo. Differential cadherin expression reflec ts, therefore, the requirement for distinct adhesive properties during different morphogenetic cell behaviors.