PUBLICATION

Maternal and zygotic activity of the zebrafish ogon locus antagonizes BMP signaling

Authors
Miller-Bertoglio, V., Carmany-Rampey, A., Fürthauer, M., Gonzalez, E.M., Thisse, C., Thisse, B., Halpern, M.E., and Solnica-Krezel, L.
ID
ZDB-PUB-990920-2
Date
1999
Source
Developmental Biology   214(1): 72-86 (Journal)
Registered Authors
Fürthauer, Maximilian, Gonzalez, Encina, Halpern, Marnie E., Solnica-Krezel, Lilianna, Thisse, Bernard, Thisse, Christine
Keywords
gastrulation; dorsal-ventral axis; ventralized mutant; maternal effect; mercedes; short tail; noggin
MeSH Terms
  • Amino Acid Sequence
  • Animals
  • Body Patterning/genetics*
  • Bone Morphogenetic Proteins/physiology*
  • Carrier Proteins
  • Chromosome Mapping*
  • Ethylnitrosourea
  • Female
  • Gene Expression Regulation, Developmental*
  • Molecular Sequence Data
  • Mutagenesis
  • Phenotype
  • Protein Biosynthesis
  • Proteins/chemistry
  • Proteins/genetics*
  • Sequence Alignment
  • Sequence Homology, Amino Acid
  • Signal Transduction
  • Zebrafish/embryology*
  • Zebrafish/genetics
  • Zygote/physiology*
PubMed
10491258 Full text @ Dev. Biol.
Abstract
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 expanded bmp2b/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 in bmp2b, is epistatic to ogom60 mutation, providing further evidence that ogo 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.
Genes / Markers
Figures
Figure Gallery
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Errata and Notes