Embryonic cells depleted of beta-catenin remain competent to differentiate into dorsal mesodermal derivatives.

Disruption of axis specification leads to defects in dorsal tissue patterning and cell movements. Here, we examine how beta-catenin coordinately affects gastrulation movements and dorsal mesoderm differentiation. The reduction of beta-catenin protein levels by morpholino oligonucleotides complementary to beta-catenin mRNA causes a disruption in gastrulation movements.