Expression of constructs of the neuronal isoform of myosin-Va interferes with the distribution of melanosomes and other vesicles in melanoma cells
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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DOI：
10.1102/cmc.10010
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发表时间：
2002-02-01
影响因子：
--
通讯作者：
Espreafico, EM
中科院分区：
文献类型：
--
作者：
Bizario, JCD;Nascimento, AAD;Espreafico, EM
肌球蛋白- va与黑色素小体易位有关，但这种功能的确切分子机制尚不清楚。在稀释的S91黑色素瘤细胞中，黑素小体向细胞周围移动，但不像野生型b16黑色素瘤细胞那样积聚在树突尖端；相反，它们主要以微管依赖的方式返回并积聚在核内体周围区域。在S91细胞中，myosin-Va全长神经元异构体的表达导致黑素小体分散，其占据的细胞面积约为未转染细胞的两倍。表明稀释表型的部分挽救。在S91细胞中，过表达完整的尾结构域并不足以诱导黑素小体分散，而是导致黑素小体聚集。B16细胞中肌球蛋白- va的头部和头颈结构域的过度表达不会改变黑素体的分布。然而，在这些细胞中，过表达完整的尾部结构域会诱导黑素小体聚集，并出现尾部相关的聚集颗粒或囊泡结构，这些结构对黑素小体和高尔基P-COP标记物表现出不同程度的染色，并与内源性肌球蛋白- va共定位。总之，目前的数据表明，肌凝蛋白- va在调节微管依赖性黑素小体易位的方向中起作用，除了如先前的研究所表明的促进黑素小体在细胞周围的捕获。这些研究也强化了肌球蛋白- v在黑素细胞中通过作用于囊泡靶向或细胞内蛋白质运输而具有更广泛功能的观点。细胞Motil。生物医学工程学报，2002。(C) 2002 Wiley-Liss, Inc。
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 B 16 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 P-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. Cell Motil. Cytoskeleton 51:57-75, 2002. (C) 2002 Wiley-Liss, Inc.