PUBLICATION

Short- and long-range functions of Goosecoid in zebrafish axis formation are independent of Chordin, Noggin 1 and Follistatin-like 1b

Authors
Dixon Fox, M., and Bruce, A.E.
ID
ZDB-PUB-090417-12
Date
2009
Source
Development (Cambridge, England)   136(10): 1675-1685 (Journal)
Registered Authors
Bruce, Ashley
Keywords
none
MeSH Terms
  • Animals
  • Animals, Genetically Modified
  • Body Patterning/physiology
  • Bone Morphogenetic Proteins/physiology
  • Carrier Proteins/physiology*
  • Embryo, Nonmammalian/physiology
  • Follistatin-Related Proteins/physiology*
  • Glycoproteins/genetics
  • Glycoproteins/physiology*
  • Goosecoid Protein/genetics
  • Goosecoid Protein/physiology*
  • Intercellular Signaling Peptides and Proteins/genetics
  • Intercellular Signaling Peptides and Proteins/physiology*
  • Mutation
  • Receptors, Notch/physiology
  • Signal Transduction/physiology
  • Zebrafish/embryology*
  • Zebrafish/physiology
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/physiology*
PubMed
19369398 Full text @ Development
Abstract
The organizer is essential for dorsal-ventral (DV) patterning in vertebrates. Goosecoid (Gsc), a transcriptional repressor found in the organizer, elicits partial secondary axes when expressed ventrally in Xenopus, similar to an organizer transplant. Although gsc is expressed in all vertebrate organizers examined, knockout studies in mouse suggested that it is not required for DV patterning. Moreover, experiments in Xenopus and zebrafish suggest a role in head formation, although a function in axial mesoderm formation is less clear. To clarify the role of Gsc in vertebrate development, we used gain- and loss-of-function approaches in zebrafish. Ventral injection of low doses of gsc produced incomplete secondary axes, which we propose results from short-range repression of BMP signaling. Higher gsc doses resulted in complete secondary axes and long-range signaling, correlating with repression of BMP and Wnt signals. In striking contrast to Xenopus, the BMP inhibitor Chordin (Chd) is not required for Gsc function. Gsc produced complete secondary axes in chd null mutant embryos and gsc-morpholino knockdown in chd mutants enhanced the mutant phenotype, suggesting that Gsc has Chd-independent functions in DV patterning. Even more striking was that Gsc elicited complete secondary axes in the absence of three secreted BMP antagonists, Chd, Follistatin-like 1b and Noggin 1, suggesting that Gsc functions in parallel with secreted BMP inhibitors. Our findings suggest that Gsc has dose dependent effects on axis induction and provide new insights into molecularly distinct short- and long-range signaling activities of the organizer.
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Human Disease / Model
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