Novel targeting strategy for generating mouse models with defects in the retinoid cycle.

In addition to RDH5, other enzymes capable of oxidizing 11-cis-retinol are present within the retinal pigment epithelium, Müller cells and/or photoreceptors. Candidate proteins have meanwhile been identified. To study the physiological and pathological aspects of these enzymes, mice in which these genes are no longer functional are being generated. A fast-targeting strategy for the disruption of genes was developed. Generation of double and triple knockouts will aid in determining if these retinol dehydrogenases are responsible for the remaining 11-cis-retinol oxidation observed in RDH5 knockout animals.