Tbx24, encoding a T-box protein, is mutated in the zebrafish somite-segmentation mutant fused somites

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Abstract
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 somites1. A large-scale screen in zebrafish previously identified five mutants that show abnormalities in somite boundary formation2. Four have essentially the same phenotype, with posterior somite defects2,3,4 and neuronal hyperplasia5,6; recent work has suggested that genes affected in these mutants encode components of the Notch signaling cascade5. The fifth mutant, fused somites (fss), shows a different phenotype characterized by complete lack of somite formation along the entire antero-posterior axis2,3. Gene expression and phenotypic analyses in mutant embryos have implicated Fss in somite formation independent of Notch signaling4,5, 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.