Meeting Abstract
Retinoic acid (RA) is a potent morphogen that patterns the anterior – posterior axis during embryonic development in vertebrates. Although key enzymatic components of the pathway are present in at least some non-vertebrate genomes, the developmental functions of retinoic acid pathway in these animals is largely unknown. We have been investigating the developmental roles of RA in our animal system, the mollusc Tritia (Ilyanassa). Our data suggest that the Tritia genome encodes copies of the RA synthesizing enzyme, RALDH, and the RA receptors, RAR and RXR, suggesting that it could have a functional RA pathway. We also recover a CYP26-like protein (Cyp26), which is predicted to degrade active RA. The morpholino (MO) knockdown of Cyp26 causes specific defects in the shell, digestive gland and the stomach. Excitingly, this is extremely similar to the effects adding RA during early shell development, indicating that it is a specific effect of excess RA in the embryo. In both treatments, the shell defect is characterized by too little shell extension, and too much shell expansion, consistent with a role for the pathway in modulating shell morphogenesis. We also knock down the predicted retinol dehydrogenase (RDH10) and find that it generally affects the same set of organs as the RA treatment and Cyp26 knockdown, further supporting a specific role for RA signaling in normal development of this embryo. Together, this is among the clearest cases known so far of developmental roles for RA signaling outside of chordates.
