Clinical studies have suggested that defects in the epaxial muscles, 
particularly multifidus, may contribute to the etiology of idiopathic scoliosis. 
While the epaxial muscles and the vertebrae derive from the same embryonic 
segmentation process, the mechanisms that pattern the multisegmental back 
muscles are still unclear. The process of segmentation is regulated by the Notch 
signaling pathway, and mutations in the modulators delta-like 3 (Dll3) and 
lunatic fringe (Lfng) are genetic models for spinal disorders such as scoliosis. 
Osteological defects have been characterized in these genetic models, but 
myological phenotypes have not previously been studied. We analyzed the 
multifidus muscle in the mouse (Mus musculus) and observed intriguing changes in 
the cranio-caudal borders of multifidus in Dll3 and Lfng models. Statistical 
analysis did not find a significant association between the majority of the 
multifidus anomalies and the vertebral defects, suggesting a previously 
unappreciated role for Notch signaling in patterning epaxial muscle groups. 
These findings indicate an additional mechanism by which DLL3 and LFNG may play 
a role in the etiology of human idiopathic scoliosis.