Members of the bone morphogenetic protein (BMP) family actively promote
ventral cell fates, such as epidermis and blood, in the vertebrate gastrula.
More dorsally, the organizer region counteracts BMP signalling through secretion
of BMP-binding antagonists chordin and noggin, allowing dorsally derived tissues
such as neurectoderm and somitic muscle to develop1. BMPs also
function in skeletal development and regeneration of bone following injury2. Noggin antagonism is thought to prevent osteogenesis at sites of
joint formation3, whereas chordin has not yet been implicated
in skeletogenesis. Analyses of zebrafish mutants have confirmed the action
of chordin (chd) in opposing ventralizing signals at gastrulation4,
5,
6. Some ventralized mutants recover and develop into fertile
adults, thereby revealing a requirement for chd function for the later
processes of fin and caudal skeletal patterning. We observe in mutants the
misexpression of genes encoding BMPs and putative downstream genes, and ectopic
sclerotomal cells. Through injections of chd mRNA into the early embryo,
we restored wild-type gene expression patterns, and the resultant fish, although
genotypically mutant, developed normal axial skeletons and fins. Our results
demonstrate that chordin function during gastrulation is important for the
correct morphogenesis of the adult zebrafish skeleton.
