Skip to main content
. Author manuscript; available in PMC: 2013 Jan 1.
Published in final edited form as: Biochim Biophys Acta. 2011 Apr 15;1821(1):198–205. doi: 10.1016/j.bbalip.2011.04.004

Table 1.

Mouse mutants for enzymes catalyzing conversion of retinol to retinoic acid (RA).

Gene Official gene name Enzyme name and activity with retinoids Major defects observed in null mutants
Adh1 Adh1 class I alcohol dehydrogenase oxidation of retinol to retinaldehyde non-lethal; adults fertile; hypersensitive to vitamin A toxicity due to reduced ability to clear excess retinol; increased retinyl esters
Adh3 Adh5 class III alcohol dehydrogenase oxidation of retinol to retinaldehyde non-lethal; adults fertile; reduced postnatal survival during vitamin A deficiency
Adh4 Adh7 class IV alcohol dehydrogenase oxidation of retinol to retinaldehyde non-lethal; adults fertile; reduced postnatal survival during vitamin A deficiency
Rdh1 Rdh1 retinol dehydrogenase-1 oxidation of retinol to retinaldehyde non-lethal; adults fertile; increased body weight, adipose tissue, and retinyl ester levels
Rdh10 Rdh10 retinol dehydrogenase-10 oxidation of retinol to retinaldehyde lethal at E13.5; craniofacial defects; small forelimbs
Raldh1 Aldh1a1 retinaldehyde dehydrogenase-1 oxidation of retinaldehyde to RA non-lethal; adults fertile; hypersensitive to vitamin A toxicity due to reduced ability to clear excess retinaldehyde; protects against obesity in adult
Raldh2 Aldh1a2 retinaldehyde dehydrogenase-2 oxidation of retinaldehyde to RA lethal at E9.5; failure in embryonic turning due to somite defect; enlarged heart; forelimb field absent; posterior hindbrain absent; posterior foregut absent
Raldh3 Aldh1a3 retinaldehyde dehydrogenase-3 oxidation of retinaldehyde to RA lethal at birth; blockage of nasal passages; mild perioptic mesenchyme defect (more severe in Raldh1;Raldh3 double knockout); forebrain LGE/striatum defects