Differential Regulation ofchordinExpression Domains in Mutant Zebrafish

AbstractPatterning along the dorsal–ventral (D–V) axis ofXenopusandDrosophilaembryos is believed to occur through a conserved molecular mechanism, with homologous proteins Chordin and Short gastrulation (Sog) antagonizing signaling by bone morphogenetic protein 4 (BMP-4) and Decapentaplegic (Dpp), respectively. We have isolated a zebrafish gene that is highly homologous tochordinandsogwithin cysteine-rich domains and exhibits conserved aspects of expression and function. As inXenopusembryos, zebrafishchordinis expressed in the organizer region and transiently in axial mesoderm. Injection of zebrafishchordinmRNA to the ventral side ofXenopusembryos induced secondary axes. Ectopic overexpression in zebrafish resulted in an expansion of paraxial mesoderm and neurectoderm at the expense of more lateral and ventral derivatives, producing a range of defects similar to those of dorsalized zebrafish mutants (Mullinset al.,1996). In accordance with the proposed function ofchordinin D–V patterning, dorsalized zebrafish mutants showed expanded domains ofchordinexpression by midgastrulation, while some ventralized mutants had reduced expression; however, in all mutants examined, early organizer expression was unaltered. In contrast toXenopus,zebrafishchordinis also expressed in paraxial mesoderm and ectoderm and in localized regions of the developing brain, suggesting that there are additional roles forchordinin zebrafish embryonic development. Surprisingly, paraxial mesodermal expression ofchordinappeared unaltered inspadetailmutants that later lack trunk muscle (Kimmelet al.,1989), while axial mesodermal expression was affected. This finding reveals an unexpected function forspadetailin midline mesoderm and in differential regulation ofchordinexpression during gastrulation