ZFIN ID: ZDB-PUB-970602-1
Loss of cerebum function ventralizes the zebrafish embryo
Fisher, S., Amacher, S.L., and Halpern, M.E.
Date: 1997
Source: Development (Cambridge, England)   124(7): 1301-1311 (Journal)
Registered Authors: Amacher, Sharon, Fisher, Shannon, Halpern, Marnie E.
Keywords: gastrulation; mesoderm; organizer; cerebum; zebrafish
MeSH Terms:
  • Alleles
  • Animals
  • Body Patterning/genetics*
  • Central Nervous System/embryology
  • Chromosome Mapping
  • Ectoderm/physiology
  • Embryonic Induction/genetics*
  • Gastrula/physiology
  • Mesoderm/physiology
  • Mutation*
  • Phenotype
  • Zebrafish/embryology
  • Zebrafish/genetics*
PubMed: 9118801
FIGURES
ABSTRACT
Recent studies implicate ventrally derived signals, in addition to dorsal ones emanating from the organizer, in patterning the vertebrate gastrula. We have identified five overlapping deficiencies that uncover the zebrafish cerebum locus and dramatically alter dorsal-ventral polarity at gastrulation. Consistent with the properties of experimentally ventralized amphibian embryos, cerebum mutants exhibit reduced neurectodermal gene expression domains and an increase in derivatives of ventral mesoderm. Structures derived from paraxial and lateral mesoderm also are reduced; however, dorsal axial mesodermal derivatives, such as the hatching gland and notochord, are largely spared. The pleiotropic action of cerebum deficiencies, and the differential response of affected tissues, suggest that the cerebum gene may normally function as an inhibitor of ventralizing signals, a function previously ascribed to Noggin and Chordin in Xenopus. Analysis of the cerebum phenotype provides genetic evidence for the existence of ventralizing signals in the zebrafish gastrula and for antagonists of those signals.
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