The T-box transcription factor, Tbx6, is essential for posterior somite formation during mouse embryogenesis. By partially restoring Tbx6expression in Tbx6 null mice, White and co-workers show, on, that Tbx6 is required for both somite specification and for proper somite rostrocaudal (RC)patterning. As somite patterning depends on Notch signalling, the authors also looked at the expression of Notch pathway genes in rescued mice, and found that Dll1 expression, which is absent in Tbx6 null mice, is restored in rescued embryos, indicating that Dll1 is a Tbx6 target. However, whether Tbx6 directly activates Dll1 remains to be proven. The authors also discovered that a spontaneous mutant, rib-vertebrae(rv), which maps near Tbx6, is a hypomorphic Tbx6mutation. Their findings, they propose, raise the possibility that some human birth defects, such as spondylocostal dysostosis, could be caused by hypomorphic mutations in TBX6 or in other components of this pathway.
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