Developmental control system of asymmetry of eye-sidedness and body coloration in flatfishes, and the mechanism that induces abnormality in the asymmetry development

我们研究了控制比目鱼外部不对称性(眼睛位置和皮肤色素沉着)的发育机制。研究表明，控制内脏器官侧性和缰核神经回路的结节信号通路(NSP)通过控制前脑不对称的形成来固定眼侧。在NSP的控制下，右旋比目鱼和左旋比目鱼在缰核和视交叉处形成相反的不对称结构。研究发现，位于背鳍底部的成体型黑素载体的前体在肌间隔中向左右两侧迁移。皮肤色素沉着的不对称性是由于在眼侧肌间隔区迁移过程中成染色质前体细胞的成熟所致。暴露于视黄酸(RA)可诱导眼侧前体细胞成熟，导致盲侧皮肤变色。

We investigated the developmental mechanism that controls external asymmetry of flatfish (eye location and skin pigmentation). It was demonstrated that the Nodal signaling pathway (NSP), which is known to control the sidedness of internal organs and neural circuit of habenulae, fixes the eye-sidedness by controlling the forebrain asymmetry formation. The dextral and sinistral flatfishes are segregated by the opposite asymmetry formation at the habenulae and optic chiasma under the control of the NSP.It was found that the precursors of adult-type melanophores that locate at the base of dorsal fin migrate in the myoseptum toward both left and right lateral sides. The asymmetry of skin pigmentation is established by the maturation of precursors to chromatoblasts during the migration in the myoseptum of the ocular side. Exposure to retinoic acid (RA) induces maturation of the precursors also in the ocular side, resulting in the coloration of blind side skin.