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首页> 外文期刊>Cell motility and the cytoskeleton >Disruption of the actin network enhances MAP-2c and Fyn-induced process outgrowth.
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Disruption of the actin network enhances MAP-2c and Fyn-induced process outgrowth.

机译：肌动蛋白网络的破坏增强了MAP-2c和Fyn诱导的过程生长。

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We investigated the interaction of MAP-2c and Fyn in the initiation of process outgrowth in COS7 cells. Single transfections of Fyn and MAP-2c resulted in a dramatic decrease in flat, rounded COS7 cells, and a significant increase in both the number of cells with multiple short, spike-like processes, and cells with longer processes. Co-transfection of Fyn and MAP-2c resulted in an additive increase in the number of cells with more than two processes and discrete sites of co-localization within processes. When single or double transfected cells were treated with cytochalasin D or lantrunculin there was a dramatic increase in the number of cells with more than two processes. In addition, there was an increase in the length of the processes, both in single and double transfected cells, suggesting that the actin meshwork provides a barrier for MT-based process extension. When co-transfected cells were post-treated with nocodazole, Fyn was not associated with MAP-2c and acetylated, stable tubulin. Although some Fyn/MAP-2c co-localization was retained, punctate staining of MAP-2c and Fyn were observed at the cell periphery, in areas devoid of stable MTs. Mutations in either tyrosine 67 (Tyr67), a site on human MAP-2c phosphorylated by Fyn, or a second tyrosine residue (Tyr50), did not alter the ability of MAP-2c and Fyn to induce process outgrowth. These studies suggest that independent of one another MAP-2c and Fyn are able to induce process outgrowth and in concert can initiate and enhance process outgrowth in an additive manner. Cell Motil. Cytoskeleton 62:110-123, 2005. (c) 2005 Wiley-Liss, Inc.
机译：我们调查了COS-2细胞中MAP-2c和Fyn在过程生长的启动中的相互作用。 Fyn和MAP-2c的单次转染导致扁平的圆形COS7细胞显着减少，具有多个短的，穗状样过程的细胞数目和具有较长过程的细胞数目均显着增加。 Fyn和MAP-2c的共转染导致具有两个以上过程以及过程中共定位离散位点的细胞数量的累加增加。当用细胞松弛素D或Lantrunculin处理单或双转染的细胞时，经过两个以上的过程，细胞数量急剧增加。另外，在单转染和双转染细胞中，过程的长度都增加了，这表明肌动蛋白网为基于MT的过程扩展提供了障碍。当用诺考达唑对共转染的细胞进行后处理时，Fyn与MAP-2c和乙酰化的稳定微管蛋白无关。尽管保留了一些Fyn / MAP-2c共定位，但是在缺乏稳定MT的区域中，在细胞外围观察到MAP-2c和Fyn的点状染色。酪氨酸67（Tyr67）（人MAP-2c上被Fyn磷酸化的位点）或第二个酪氨酸残基（Tyr50）中的突变都不会改变MAP-2c和Fyn诱导过程生长的能力。这些研究表明，MAP-2c和Fyn彼此独立，能够诱导过程产物生长，并且可以以相加的方式共同引发和增强过程产物生长。细胞动力。 Cytoskeleton 62：110-123，2005.（c）2005 Wiley-Liss，Inc.

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