Regulation of the stability of beta catenin protein is a critical role of W
nt signaling cascades. In early Xenopus development, dorsal axis specificat
ion depends on regulation of beta catenin by both cytoplasmic and nuclear m
echanisms. While the cytoplasmic protein axin is known as a key component o
f the cytoplasmic beta catenin degradation complex, loss-of-function studie
s are needed to establish whether it is required for dorso-ventral patterni
ng in the embryo, and to test where in the embryo it carries out its functi
on. Here, we show that embryos lacking maternal axin protein have increased
levels of soluble beta catenin protein and increased nuclear localization
of beta catenin in ventral nuclei at the blastula stage. These embryos gast
rulate abnormally and develop with excessive notochord and head structures,
and reduced tail and ventral components. They show increased expression of
dorsal markers, including siamois, Xnr3, chordin, gsc, Xhex, and Otx2, dec
reased expression of Xwnt 8 and Xbra, and little alteration of BMP4 and Xve
nt1 and -2 mRNA levels. The ventral halves of axin-depleted embryos at the
gastrula stage have dramatically increased levels of chordin expression, an
d severely decreased levels of Xwnt 8 mRNA expression, while BMP4 transcrip
t levels are only slightly reduced. This dorso-anterior phenotype is rescue
d by axin mRNA injected into the vegetal pole of axin-depleted oocytes befo
re fertilization. Interestingly, the phenotype was rescued by ventral but n
ot dorsal injection of axin mRNA, at the 4-cell stage, although dorsal inje
ction into wild-type embryos does cause ventralization. These results show
directly that the localized ventral activity of maternal axin is critical f
or the correct patterning of the early Xenopus embryo. (C) 2001 Academic Pr
ess.