Flatfish, such as flounder and sole, are characterized by an asymmetric morphology. Once develop symmetrically like ordinary fish, they transform into an asymmetric body plan during metamorphosis. One eye migrates to the other side and pigment cells differentiate only on the ocular side, resulting in asymmetric body coloration. It has shown that thyroid hormone induces the flatfish metamorphosis, however, little is known how metamorphic morphogenesis is regulated.

Several flatfish species are active target for aquaculture production as they have high market value, however, abnormal morphology and/or coloration are problematic. We would like to understand the molecular mechanism of flatfish metamorphosis and contribute to reducing such problems that occur in aquaculture.

To address the biological questions of flatfish metamorphosis, we are using medaka and zebrafish as experimental model organisms for gene function analysis. These small fish are widely used as experimental model organisms due to their excellent characteristics: ease of maintenance and breeding as well as variety of experimental options, including genome editing. We isolate the medaka version (ortholog) of a gene of interest, for example, a gene involved in flatfish metamorphosis, then investigate gene function using the experimental model system. There are, however, many metamorphosis-related phenomena that can only be observed in flatfish. Thus, we are also trying to develop experimental methods to examine gene function in non-conventional model, flatfish, in which there are limitations to apply experimental techniques.