Ventralizing transcriptional repressors in the Vox/Vent family have been pr
oposed to be important regulators of dorsoventral patterning in the early e
mbryo, While the zebrafish genes vox (vega1) and vent (vega2) both have ven
tralizing activity in overexpression assays, loss-of function studies are n
eeded to determine whether these genes have distinct or redundant functions
in dorsoventral patterning and to provide critical tests of the proposed r
egulatory interactions among vex, vent and other genes that act to establis
h the dorsoventral axis. We show that vox and vent are redundant repressors
of dorsal fates in zebrafish. Mutants that lack vox function have little o
r no dorsoventral patterning defect, and inactivation of either vox or vent
by injection of antisense morpholino oligonucleotides has little or no eff
ect on the embryo. In contrast, embryos that lack both vox and vent functio
n have a dorsalized phenotype, Expression of dorsal mesodermal genes, inclu
ding chordin, goosecoid and bozozok, is strongly expanded in embryos that l
ack vox and vent function, indicating that the redundant action of vox and
vent is required to restrict dorsal genes to their appropriate territories,
Our genetic analysis indicates that the dorsalizing transcription factor B
ozozok promotes dorsal fates indirectly, by antagonizing the expression of
vox and vent. In turn, vox and vent repress chordin expression, restricting
its function as an antagonist of ventral fates to the dorsal side of the e
mbryo, Our results support a model in which BMP signaling induces the expre
ssion of ventral genes, while vox and vent act redundantly to prevent the e
xpression of chordin, goosecoid and other dorsal genes in the lateral and v
entral mesendoderm.