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Neural tube defects (NTDs), one of the most common birth defects in human, present a multifactorial etiology with a poorly defined genetic component. The  Dlx5  and  Dlx6  bigenic cluster encodes two evolutionary conserved homeodomain transcription factors, which are necessary for proper vertebrate development. It has been shown that  Dlx5/6  genes are essential for anterior neural tube closure, however their role in the formation of the posterior structures has never been described. Here, we show that  Dlx5/6  expression is required during vertebrate posterior axis formation.  Dlx5  presents a similar expression pattern in neural plate border cells during posterior neurulation of zebrafish and mouse.  Dlx5/6 -inactivation in the mouse results in a phenotype reminiscent of NTDs characterized by open thoracic and lumbar vertebral arches and failure of epaxial muscle formation at the dorsal midline. The  dlx5a/6a  zebrafish morphants present posterior NTDs associated with abnormal delamination of neural crest cells showing altered expression of cell adhesion molecules and defects of motoneuronal development. Our findings provide new molecular leads to decipher the mechanisms of vertebrate posterior neurulation and might help to gather a better understanding of human congenital NTDs etiology.

Posterior axis formation requires Dlx5/Dlx6 expression at the neural plate border