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首页> 外文期刊>Journal of cellular physiology. >The PRMT5/HURP axis retards Golgi repositioning by stabilizing acetyl-tubulin and Golgi apparatus during cell migration
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The PRMT5/HURP axis retards Golgi repositioning by stabilizing acetyl-tubulin and Golgi apparatus during cell migration

机译：PRMT5 / HURP轴阻碍高尔基重新定位稳定acetyl-tubulin和高尔基体在细胞迁移

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摘要

The Golgi apparatus (GA) translocates to the cell leading end during directional migration, thereby determining cell polarity and transporting essential factors to the migration apparatus. The study provides mechanistic insights into how GA repositioning (GR) is regulated. We show that the methyltransferase PRMT5 methylates the microtubule regulator HURP at R122. The HURP methylation mimicking mutant 122F impairs GR and cell migration. Mechanistic studies revealed that HURP 122F or endogenous methylated HURP, that is, HURP m122, interacts with acetyl-tubulin. Overexpression of HURP 122F stabilizes the bundling pattern of acetyl-tubulin by decreasing the sensitivity of the latter to a microtubule disrupting agent nocodazole. HURP 122F also rigidifies GA via desensitizing the organelle to several GA disrupting chemicals. Similarly, the acetyl-tubulin mimicking mutant 40Q or tubulin acetyltransferase αTAT1 can rigidify GA, impair GR, and retard cell migration. Reversal of HURP 122F-induced GA rigidification, by knocking down GA assembly factors such as GRASP65 or GM130, attenuates 122F-triggered GR and cell migration. Remarkably, PRMT5 is found downregulated and the level of HURP m122 is decreased during the early hours of wound healing-based cell migration, collectively implying that the PRMT5-HURP-acetyl-tubulin axis plays the role of brake, preventing GR and cell migration before cells reach empty space.
机译：高尔基体(GA)把细胞前端在定向迁移,从而确定细胞极性和运输要素迁移设备。研究提供了机械的深入了解重新定位(GR)监管。甲基转移酶PRMT5混入甲醇的微管调节器HURP R122。甲基化模仿122 f损害GR和突变细胞迁移。HURP 122 f或内源性甲基化HURP,也就是说,HURP m122,与acetyl-tubulin交互。超表达HURP 122 f稳定捆绑销售的模式acetyl-tubulin减少后者的敏感性微管扰乱代理诺考达唑。固定GA通过减感作用的细胞器几个GA破坏的化学物质。acetyl-tubulin模仿突变40问或微管蛋白乙酰转移酶αTAT1可以固定GA,损害GR,阻碍细胞迁移。122年f-induced GA僵化,击倒GA组装GRASP65或GM130等因素,122年变弱f-triggered GR和细胞迁移。值得注意的是,发现PRMT5表达下调和在早期的水平HURP m122却降低了小时的伤口healing-based细胞迁移,集体暗示PRMT5-HURP-acetyl-tubulin轴的角色制动,防止GR和细胞迁移细胞达到空的空间。

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