Mechanisms of eye relocation during flatfish metamorphosis, - asymmetrical morphogenesis by thyroid hormone

比目鱼的外部不对称性在动物界中最为显著。对称幼虫的一只眼移向对侧，有双眼的一侧在变态过程中，尤其是在甲状腺激素（TH）的控制下，比目鱼的眼侧（眼侧）通过成体型黑色素细胞（aMLP）的表达而变暗。（盲侧），同时发展的过程中眼睛迁移变态。由于铅需要TH在一个特定的时间，TH的参与表明在盲侧的形成。从体内和体外实验中，这表明，TH也发挥作用，通过抑制自发表达的aMLP的盲侧的着色。为了回答这个问题，为什么TH可以发挥其作用，只有在未来的盲侧，在不同的时间，TH处理的斑点比目鱼的幼虫人工变态。在TH的作用下，无论是太早还是太晚，变态都会增加“ambicoloration”（两侧的眼侧特征）的发生。另一方面，在特定的时间，TH的作用下，观察到“假白化”（两侧的盲侧特征）。在此基础上，估计了TH诱发盲侧特性的反应性。左侧（正常青少年的盲侧）的反应期长于右侧，这种差异被认为是变态不对称的中心机制。

The external asymmetry of flatfish is most significant in the animal kingdom. One eye of the symmetrical larva migrates to the opposite side, and the side with both eyes (ocular side) becomes dark by the expression of the adult-type melanophores(aMLP) during metamorphosis, particularly under the control of thyroid hormones(THs).The pseudomesial bar(Pb), a unique bone that is present in flatfish only on the side without eyes (blind side), simultaneously developed with the progress of eye migration during metamorphosis. Since Pb required TH at a specific time, the involvement of TH was indicated in the formation of the blind side. From in vivo and in vitro experiments, it was suggested that TH also plays a role in the coloration of the blind side by suppressing the spontaneous expression of aMLP.To answer the question why TH can exert its effect only on the future blind side, the larvae of spotted halibut were artificially metamorphosed by TH treatment at various timings. The occurrence of "ambicoloration" (ocular-side characteristic on both the sides) was increased by metamorphosis under the action of TH that was either too early or too late. On the other hand, "pseudoalbino" (blind-side characteristic on both sides) was observed under the action of TH at a specific time. Based on the results, TH responsiveness to induce blind-side characteristic was estimated. The responsive period was longer for the left side (blind side in the normal juveniles) than for the right side, and this difference was believed to be the central mechanism for the metamorphic asymmetry.