The early patterning of mesoderm in the Xenopus embryo requires signal
s from several intercellular factors, including mesoderm-inducing agen
ts that belong to the fibroblast growth factor (FGF) and TGF-beta fami
lies. In animal hemisphere explants (animal caps), basic FGF and the T
GF-beta family member activin are capable of converting pre-ectodermal
cells to a mesodermal fate, although activin is much more effective a
t inducing dorsal and anterior mesoderm than is basic FGF. Using a dom
inant-negative form of the Xenopus type 1 FGF receptor, we show that a
n FGF signal is required for the full induction of mesoderm by activin
. Animal caps isolated from embryos that have been injected with the t
runcated FGF receptor and cultured with activin do not extend and the
induction of some genes, including cardiac actin and Xbra, is greatly
diminished, while the induction of other genes, including the head org
anizer-specific genes gsc and Xlim-1, is less sensitive. These results
are consistent with the phenotype of the truncated FGF receptor-injec
ted embryo and imply that the activin induction of mesoderm depends on
FGF, with some genes requiring a higher level of FGF signaling than o
thers.