We have investigated the function of the retinoic acid metabolising enzyme, CYP26B1, by administering an antisense morpholino oligonucleotide to zebrafish embryos. The result was an alteration in the morphology of the embryo in those regions which express the gene, namely an embryo with a smaller head, correspondingly smaller hindbrain rhombomeres and severely reduced numbers of vagal brachiomotor neurons. Most strikingly, these embryos had defective or absent jaw cartilages implying a role for this enzyme in patterning or migration of the neural crest cells which give rise to this tissue type. In order to determine whether this phenotype resembles that of excess retinoic acid or a deficiency of retinoic acid, we compared the jaw defects following retinoic acid treatment or DEAB treatment, the latter being an inhibitor of retinoic acid synthesis. The effects of the inhibitor rather than excess retinoic acid most closely phenocopied the jaw defects seen with the Cyp26B1 morpholino which suggests that, at least in the zebrafish embryo, the action of CYP26B1 in the neural crest may not be simply to catabolise all-trans-RA.