Tbx24, encoding a T-box protein, is mutated in the zebrafish somite-segmentation mutant fused somites
- Nikaido, M., Kawakami, A., Sawada, A., Furutani-Seiki, M., Takeda, H., and Araki, K.
- Nature Genetics 31(2): 195-199 (Journal)
- Registered Authors
- Araki, Kazuo, Furutani-Seiki, Makoto, Kawakami, Atsushi, Nikaido, Masataka, Sawada, Atsushi, Takeda, Hiroyuki
- MeSH Terms
- Amino Acid Sequence
- Cell Differentiation/genetics
- Chromosome Mapping
- Gene Expression Regulation, Developmental
- Molecular Sequence Data
- T-Box Domain Proteins/genetics*
- Zebrafish Proteins/genetics*
- 12021786 Full text @ Nat. Genet.
Nikaido, M., Kawakami, A., Sawada, A., Furutani-Seiki, M., Takeda, H., and Araki, K. (2002) Tbx24, encoding a T-box protein, is mutated in the zebrafish somite-segmentation mutant fused somites. Nature Genetics. 31(2):195-199.
Somites are fundamental structures within the paraxial mesoderm of the vertebrate embryo that give rise to the vertebrae and muscle of the trunk and tail. Studies of knockout mice and gene expression analyses have shown that the Notch pathway is crucial in establishing the reiterative pattern of somites. A large-scale screen in zebrafish previously identified five mutants that show abnormalities in somite boundary formation. Four have essentially the same phenotype, with posterior somite defects and neuronal hyperplasia; recent work has suggested that genes affected in these mutants encode components of the Notch signaling cascade. The fifth mutant, fused somites (fss), shows a different phenotype characterized by complete lack of somite formation along the entire antero-posterior axis. Gene expression and phenotypic analyses in mutant embryos have implicated Fss in somite formation independent of Notch signaling, suggesting the presence of a new pathway regulating somite boundary formation. We show here that the fss gene encodes a T-box transcription factor that is expressed in intermediate to anterior presomitic mesoderm (PSM) and is involved in PSM maturation.
Genes / Markers
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Engineered Foreign Genes