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首页> 外文期刊>Cell motility and the cytoskeleton >Expression of constructs of the neuronal isoform of myosin-Va interferes with the distribution of melanosomes and other vesicles in melanoma cells.
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Expression of constructs of the neuronal isoform of myosin-Va interferes with the distribution of melanosomes and other vesicles in melanoma cells.

机译：肌球蛋白-Va神经元亚型的构建体表达干扰黑素瘤细胞中黑素体和其他囊泡的分布。

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Myosin-Va has been implicated in melanosome translocation, but the exact molecular mechanisms underlying this function are not known. In the dilute, S91 melanoma cells, melanosomes move to the cell periphery but do not accumulate in the tips of dendrites as occurs in wild-type B16 melanocytes; rather, they return and accumulate primarily at the pericentrosomal region in a microtubule-dependent manner. Expression of the full-length neuronal isoform of myosin-Va in S91 cells causes melanosomes to disperse, occupying a cellular area approximately twice that observed in non-transfected cells, suggesting a partial rescue of the dilute phenotype. Overexpression of the full tail domain in S91 cells is not sufficient to induce melanosome dispersion, rather it causes melanosomal clumping. Overexpression of the head and head-neck domains of myosin-Va in B16 cells does not alter the melanosome distribution. However, overexpression of the full tail domain in these cells induces melanosome aggregation and the appearance of tail-associated, aggregated particles or vesicular structures that exhibit variable degrees of staining for melanosomal and Golgi beta-COP markers, as well as colocalization with the endogenous myosin-Va. Altogether, the present data suggest that myosin-Va plays a role in regulating the direction of microtubule-dependent melanosome translocation, in addition to promoting the capture of melanosomes at the cell periphery as suggested by previous studies. These studies also reinforce the notion that myosin-V has a broader function in melanocytes by acting on vesicular targeting or intracellular protein trafficking.
机译：肌球蛋白-Va与黑素体易位有关，但尚不清楚该功能的确切分子机制。在稀的S91黑色素瘤细胞中，黑素体移至细胞外围，但不像野生型B16黑色素细胞那样在树突尖端聚集。相反，它们主要以微管依赖性方式返回并聚集在中心体区域。肌球蛋白-Va的全长神经元同工型在S91细胞中的表达导致黑素体分散，占据的细胞面积大约是未转染细胞中观察到的两倍，这表明该稀表型得以部分挽救。 S91细胞中完整尾部结构域的过表达不足以诱导黑素体分散，而是引起黑素体团块。 B16细胞中肌球蛋白-Va的头和头颈部域的过度表达不会改变黑素体的分布。但是，这些细胞中完整尾部结构域的过表达会诱导黑素体聚集，并出现与尾部相关的聚集颗粒或水泡结构，这些结构对黑素体和高尔基β-COP标记的染色程度不同，并与内源性肌球蛋白共定位-Va。总之，目前的数据表明，肌球蛋白-Va除调节如前研究所述的促进黑素体在细胞周围的捕获外，还起着调节微管依赖性黑素体易位的作用。这些研究还强化了一种观点，即肌球蛋白-V通过作用于囊泡靶向或细胞内蛋白运输而在黑素细胞中具有更广泛的功能。

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