Skin pigment pattern formation in zebrafish requires pigment-cell autonomous interactions between melanophores and xanthophores, yet the molecular bases for these interactions remain largely unknown. Here, we examined the dali mutant that exhibits stripes in which melanophores are intermingled abnormally with xanthophores. By in vitro cell culture, we found that melanophores of dali mutants have a defect in motility and that interactions between melanophores and xanthophores are defective as well. Positional cloning and rescue identified dali as tetraspanin 3c (tspan3c), encoding a transmembrane scaffolding protein expressed by melanophores and xanthophores. We further showed that dali mutant Tspan3c expressed in HeLa cell exhibits a defect in N-glycosylation and is retained inappropriately in the endoplasmic reticulum. Our results are the first to identify roles for a tetraspanin superfamily protein in skin pigment pattern formation and suggest new mechanisms for the establishment and maintenance of zebrafish stripe boundaries.

中文翻译：

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Tetraspanin 3c 对斑马鱼成年色素条纹中色素细胞相互作用和边界形成的要求。

斑马鱼皮肤色素模式的形成需要黑素细胞和黄素之间的色素细胞自主相互作用，但这些相互作用的分子基础仍然很大程度上未知。在这里，我们检查了表现出条纹的 dali 突变体，其中黑色素细胞与黄素异常混合。通过体外细胞培养，我们发现 dali 突变体的黑素细胞存在运动缺陷，黑素细胞和黄体之间的相互作用也存在缺陷。定位克隆和拯救将 dali 鉴定为四跨膜蛋白 3c (tspan3c)，编码由黑素细胞和黄素表达的跨膜支架蛋白。我们进一步表明，在 HeLa 细胞中表达的 dali 突变体 Tspan3c 表现出 N-糖基化缺陷，并且不恰当地保留在内质网中。