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首页> 外文期刊>Molecular biology of the cell >Myosin motors and not actin comets are mediators of the actin-based Golgi-to-endoplasmic reticulum protein transport
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Myosin motors and not actin comets are mediators of the actin-based Golgi-to-endoplasmic reticulum protein transport

机译：肌球蛋白运动而不是肌动蛋白彗星是基于肌动蛋白的高尔基体向内质网蛋白运输的介质

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We have previously reported that actin filaments are involved in protein transport from the Golgi complex to the endoplasmic reticulum. Herein, we examined whether myosin motors or actin comets mediate this transport. To address this issue we have used, on one hand, a combination of specific inhibitors such as 2,3-butanedione monoxime (BDM) and 1-[5-isoquinoline sulfonyl]-2-methyl piperazine (ML7), which inhibit myosin and the phosphorylation of myosin 11 by the myosin light chain kinase, respectively; and a mutant of the nonmuscle myosin 11 regulatory light chain, which cannot be phosphorylatod (MRLC2(AA)). On the other hand, actin comet tails were induced by the-overexpression of phosphatidylinositol phosphate 5-kinase. Cells treated with BDM/ML7 or those that express the MRLC2(AA) mutant revealed a significant reduction in the brefeldin A (BFA)-induced fusion of Golgi enzymes with the endoplasmic reticulum (ER). This delay was not caused by an alteration in the formation of the BFA-induced tubules from the Golgi complex. In addition, the Sh figa toxin fragment B transport from the Golgi complex to the ER was also altered. This impairment in the retrograde protein transport was not due to depletion of intracellular calcium stores or to the activation of Rho kinase. Neither the reassembly of the Golgi complex after BFA removal nor VSV-G transport from ER to the Golgi was altered in cells treated with BDM/ML7 or expressing MRLC2(AA). Finally, transport carriers containing Shiga toxin did not move into the cytosol at the ' tips of comet tails of polymerizing actin. Collectively, the results indicate that 1) myosin motors move to transport carriers from the Golgi complex to the ER along actin filaments; 2) nonmuscle myosin II mediates in this process; and 3) actin comets are not involved in retrograde transport. [References: 78]
机译：以前我们已经报道过肌动蛋白丝参与了从高尔基体到内质网的蛋白运输。在这里，我们检查了肌球蛋白电机或肌动蛋白彗星是否介导这种运输。为了解决这个问题，我们一方面使用了特定抑制剂的组合，例如2,3-丁二酮单肟（BDM）和1- [5-异喹啉磺酰基] -2-甲基哌嗪（ML7），它们抑制肌球蛋白和肌球蛋白轻链激酶分别使肌球蛋白11磷酸化;以及非肌肉肌球蛋白11调节轻链的突变体，该突变体不能被磷酸化（MRLC2（AA））。另一方面，肌动蛋白彗星尾巴是由磷脂酰肌醇磷酸5-激酶的过表达诱导的。用BDM / ML7处理的细胞或表达MRLC2（AA）突变的细胞显示，布雷菲德菌素A（BFA）诱导的高尔基酶与内质网（ER）融合显着减少。这种延迟不是由高尔基复合体中BFA诱导的小管形成的改变引起的。此外，Sh figa毒素片段B从高尔基体到ER的转运也被改变。逆行蛋白质运输中的这种损害不是由于细胞内钙存储的耗尽或Rho激酶的活化引起的。在用BDM / ML7处理或表达MRLC2（AA）的细胞中，去除BFA后高尔基复合体的重组和从ER向高尔基的VSV-G转运都没有改变。最后，含有志贺毒素的运输载体没有在聚合肌动蛋白彗尾的尖端移入胞质溶胶。总体而言，结果表明：1）肌球蛋白电动机运动，以沿肌动蛋白丝将载体从高尔基复合体转运至内质网; 2）非肌肉肌球蛋白II在此过程中介导; 3）肌动蛋白彗星不参与逆行运输。 [参考：78]

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