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Uveal coloboma is a potentially blinding congenital ocular malformation caused by failure of the optic fissure to close during development. Although mutations in numerous genes have been described, these account for a minority of cases, complicating molecular diagnosis and genetic counseling. Here we describe a key role of  aldh7a1  as a gene necessary for normal eye development. We show that morpholino knockdown of  aldh7a1  in zebrafish causes uveal coloboma and misregulation of  nlz1 , another known contributor to the coloboma phenotype, as well as skeletal abnormalities. Knockdown of  aldh7a1  leads to reduced cell proliferation in the optic cup of zebrafish, delaying the approximation of the edges of the optic fissure. The  aldh7a1  morphant phenotype is partially rescued by co-injection of  nlz1  mRNA suggesting that  nlz1  is functionally downstream of  aldh7a1  in regulating cell proliferation in the optic cup. These results support a role of  aldh7a1  in ocular development and skeletal abnormalities in zebrafish.

aldh7a1 Regulates Eye and Limb Development in Zebrafish