Somitogenesis is a complex process during early vertebrate development involving 
interactions between many factors to form a bilateral somite series. A role for 
chromatin remodelers in somitogenesis has not yet been demonstrated. Here, we 
investigate the function of chromodomain helicase DNA binding protein 7 (chd7) 
during zebrafish somitogenesis. We show that Chd7 deficiency leads to asymmetric 
segmentation of the presomitic mesoderm (PSM), as revealed by expression of the 
somitogenesis genes, cdx1a, dlc, her7, mespa, and ripply1. Moreover, we show 
that abrogation of Chd7 results in the loss of asymmetric expression of spaw in 
the lateral plate mesoderm, which is consistent with more general laterality 
defects. Based on the observation that insufficient Chd7 leads to left-right 
asymmetry defects during PSM segmentation, and because CHD7 has been linked to 
human spinal deformities, we suggest that zebrafish chd7 morphants may be a good 
in vivo model to examine the pathophysiology of these diseases.