Maternal and Zygotic Activity of the Zebrafish ogon Locus Antagonizes BMP Signaling

The dorsal–ventral axis of vertebrate embryos is thought to be specified by a gradient of bone morphogenetic protein (BMP) activity, which, in part, arises through the interaction of dorsally expressed antagonists Chordin and Noggin with the ventralizing BMPs. The zebrafish mercedestm305, ogonm60, and short tailb180 mutations produce ventralized phenotypes, including expandedbmp2b/4 expression domains. We find that the three mutations are allelic and that the locus they define, renamed ogon (ogo), maps to linkage group 25. The ogom60 and ogob180 mutations are deficiencies and thus represent null alleles, whereas the ENU-induced allele ogotm305 retains partial function. Aspects of the ogom60 and ogotm305 mutant phenotypes are fully suppressed by overexpression of BMP antagonists. Moreover, swirltc300, a null mutation inbmp2b, is epistatic to ogom60 mutation, providing further evidence thatogo normally functions in a BMP-dependent manner. Embryonic patterning is highly sensitive to maternal and zygotic ogo gene dosage, especially when the level of zygotic chordin activity is also reduced. However, elimination of the zygotic activity of both genes does not result in a completely ventralized embryo. Thus, while ogo and chordin are required to limit activity of BMPs, additional mechanisms must exist to block these ventralizing signals. We have ruled out zebrafish noggin homologues as candidates for the ogo gene, including a newly identified gene, nog1, which is specifically expressed in the gastrula organizer. The results suggest that ogo encodes an as yet unidentified dorsalizing factor that mediates dorsoventral patterning by directly or indirectly antagonizing BMP activity.