Maternal-zygotic medaka mutants for fgfr1 reveal its essential role in the migration of the axial mesoderm but not the lateral mesoderm.

The medaka fish (Oryzias latipes) is an emerging model organism for which a variety of unique developmental mutants have now been generated. Our recent mutagenesis screening of the medaka identified headfish (hdf), a null mutant for fgf receptor 1 (fgfr1), which fails to develop structures in the trunk and tail. Despite its crucial role in early development, the functions of Fgfr1-mediated signaling have not yet been well characterized due to the complexity of the underlying ligand-receptor interactions. In our present study, we further elucidate the roles of this pathway in the medaka using the hdf (fgfr1) mutant. Because Fgfr1 is maternally supplied in fish, we first generated maternal-zygotic (MZ) mutants by transplanting homozygous hdf germ cells into sterile interspecific hybrids. Interestingly, the host hybrid fish recovered their fertility and produced donor-derived mutant progeny. The resulting MZ mutants also exhibited severe defects in their anterior head structures that are never observed in the corresponding zygotic mutants. A series of detailed analyses subsequently revealed that Fgfr1 is required for the anterior migration of the axial mesoderm, particularly the prechordal plate, in a cell-autonomous manner, but is not required for convergence movement of the lateral mesoderm. Furthermore, fgfr1 was found to be dispensable for initial mesoderm induction. The MZ hdf medaka mutant was thus found to be a valuable model system to analyze the precise role of fgfr1-mediated signaling in vertebrate early development.