PUBLICATION

no tail (ntl) is the zebrafish homologue of the mouse T (Brachyury) gene

Authors
Schulte-Merker, S., van Eeden, F.J.M., Halpern, M.E., Kimmel, C.B., and Nüsslein-Volhard, C.
ID
ZDB-PUB-961014-1010
Date
1994
Source
Development (Cambridge, England)   120: 1009-1015 (Journal)
Registered Authors
Halpern, Marnie E., Kimmel, Charles B., Nüsslein-Volhard, Christiane, Schulte-Merker, Stefan, van Eeden, Freek
Keywords
none
MeSH Terms
  • Amino Acid Sequence
  • Animals
  • Base Sequence
  • Blotting, Southern
  • Blotting, Western
  • DNA-Binding Proteins/genetics*
  • Fetal Proteins/genetics*
  • Genome
  • Immunohistochemistry
  • In Situ Hybridization
  • Mesoderm/physiology*
  • Mice
  • Molecular Sequence Data
  • Mutation
  • Notochord/cytology
  • Notochord/physiology
  • T-Box Domain Proteins*
  • Zebrafish/genetics*
  • Zebrafish Proteins*
PubMed
7600949
Abstract
The mouse T (Brachyury) gene is required for normal mesoderm development and the extension of the body axis. Recently, two mutant alleles of a zebrafish gene, no tail (ntl), have been isolated (Halpern, M. E., Ho., R. K., Walker, C. and Kimmel, C. B. (1993) Cell 75, 99-111). ntl mutant embryos resemble mouse T/T mutant embryos in that they lack a differentiated notochord and the caudal region of their bodies. We report here that this phenotype is caused by mutation of the zebrafish homologue of the T gene. While ntl embryos express mutant mRNA, they show no nuclear protein product. Later, expression of mRNA in mutants, but not in wild types, is greatly reduced along the dorsal midline where the notochord normally forms. This suggests that the protein is required for maintaining transcription of its own gene.
Genes / Markers
Figures
Figure Gallery
Expression
Phenotype
Mutation and Transgenics
Human Disease / Model Data
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping
Errata and Notes