ZFIN ID: ZDB-PUB-080212-1
Noggin1 and Follistatin-like2 function redundantly to Chordin to antagonize BMP activity
Dal-Pra, S., Fürthauer, M., Van-Celst, J., Thisse, B., and Thisse, C.
Date: 2006
Source: Developmental Biology 298(2): 514-526 (Journal)
Registered Authors: Dal-Pra, Sophie, Fürthauer, Maximilian, Thisse, Bernard, Thisse, Christine, Van Celst, Jeanne
Keywords: Zebrafish, Gastrulation, Dorso-ventral axis, BMP, noggin, chordin, ogon, follistatin, follistatin-like
MeSH Terms:
  • Animals
  • Base Sequence
  • Body Patterning*
  • Bone Morphogenetic Proteins/antagonists & inhibitors
  • Bone Morphogenetic Proteins/physiology*
  • Carrier Proteins/genetics
  • Carrier Proteins/physiology*
  • Embryo, Nonmammalian
  • Follistatin/genetics
  • Follistatin-Related Proteins/physiology*
  • Gene Expression Regulation, Developmental
  • Glycoproteins/genetics
  • Glycoproteins/physiology*
  • Intercellular Signaling Peptides and Proteins/genetics
  • Intercellular Signaling Peptides and Proteins/physiology*
  • Molecular Sequence Data
  • RNA/genetics
  • Zebrafish/embryology*
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology*
PubMed: 16890217 Full text @ Dev. Biol.
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ABSTRACT
In Xenopus, the dorso-ventral (D/V) axis is thought to be specified by the bone morphogenetic proteins (Bmp) activity arising through interaction with antagonists such as Noggin, Chordin and Follistatin. We report here, through inactivation of noggin1 (nog1) that this gene is not essential by itself to establish the D/V patterning. However, at blastula stage, inactivation of nog1 strongly amplifies chordin (chd) phenotype, revealing redundant functions of these two genes on D/V axis formation. Substantial dorsal tissues remaining in the double nog1-chd morphant suggested that other anti-Bmp factors may pattern the D/V axis. We isolated two potential candidates, the follistatin-like (fstl) genes. We found that fstl2 is an early gastrula expressed gene. Its inactivation, similar to nog1, strongly enhances the chd phenotype. Moreover, the penetrance of the ventralization phenotype is much higher when we inactivated simultaneously chd, nog1 and fstl2. Altogether, our data reveal that, while Chordin is the main player of the D/V axis, sufficient to maintain proper activity of Bmp gradient, the structures remaining in the chd mutant (namely dorsal and dorso-lateral territories, in both mesodermal and ectodermal layers) result from the anti-Bmp activity carried by Nog1 and Fstl2 at blastula and gastrula stages.
ADDITIONAL INFORMATIONNo data available