no tail (ntl) is the zebrafish homologue of the mouse T (Brachyury) gene
- Schulte-Merker, S., van Eeden, F.J.M., Halpern, M.E., Kimmel, C.B., and Nüsslein-Volhard, C.
- Development (Cambridge, England) 120: 1009-1015 (Journal)
- Registered Authors
- Halpern, Marnie E., Kimmel, Charles B., Nüsslein-Volhard, Christiane, Schulte-Merker, Stefan, van Eeden, Freek
- MeSH Terms
- Amino Acid Sequence
- Base Sequence
- Blotting, Southern
- Blotting, Western
- DNA-Binding Proteins/genetics*
- Fetal Proteins/genetics*
- In Situ Hybridization
- Molecular Sequence Data
- T-Box Domain Proteins*
- Zebrafish Proteins*
- 7600949 Full text @ Development
Schulte-Merker, S., van Eeden, F.J.M., Halpern, M.E., Kimmel, C.B., and Nüsslein-Volhard, C. (1994) no tail (ntl) is the zebrafish homologue of the mouse T (Brachyury) gene. Development (Cambridge, England). 120:1009-1015.
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
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes