DIFFERENTIAL EFFECT OF MONENSIN ON ENVELOPED VIRUSES THAT FORM AT DISTINCT PLASMA-MEMBRANE DOMAINS
DIFFERENTIAL EFFECT OF MONENSIN ON ENVELOPED VIRUSES THAT FORM AT DISTINCT PLASMA-MEMBRANE DOMAINS
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DOI：
10.1083/jcb.89.3.700
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发表时间：
1981-01-01
影响因子：
7.8
通讯作者：
COMPANS, RW
中科院分区：
文献类型：
--
作者：
ALONSO, FV;COMPANS, RW
离子载体莫能菌素对流感病毒和水疱性口炎病毒（VSV）在Madin-Darby犬肾（MDCK）和幼鼠肾（BHK-21）细胞中的复制有显著不同的影响。在MDCK细胞中，流感病毒在根尖表面组装，而VSV颗粒从基底外侧膜芽出；而在BHK-21细胞中则没有这种成熟极性。与对照组相比，10-6 M浓度的莫能菌素可使MDCK细胞中的VSV产量降低约90%，而流感病毒产量不受影响。在BHK-21细胞中，莫能菌素也能抑制VSV的产生，但流感病毒对离子载体也很敏感。固定和未固定MDCK单层的免疫荧光染色表明，VSV糖蛋白在莫能菌素存在下合成，但其在质膜上的出现被阻断。用莫能菌素处理的VSV感染的MDCK细胞的电镜显示VSV颗粒聚集在扩张的细胞质囊泡内。莫能菌素处理的流感病毒感染的MDCK细胞也含有扩张的细胞质囊泡，但在这些结构中没有发现病毒颗粒，并且在细胞表面观察到许多流感病毒粒子出芽。莫能菌素治疗显然不能阻断流感病毒糖蛋白的转运；VSV - G蛋白的运输明显受阻。MDCK细胞中存在至少2种不同的糖蛋白转运到质膜的途径，其中1种途径被莫能菌素阻断。
A striking differential effect of the ionophore, monensin was observed on replication of influenza virus and vesicular stomatitis virus (VSV) in Madin-Darby canine kidney (MDCK) and baby hamster kidney (BHK-21) cells. In MDCK cells, influenza virus is assembled at the apical surfaces, whereas VSV particles bud from the basolateral membranes; no such polarity of maturation is exhibited in BHK-21 cells. A 10-6 M concentration of monensin reduces VSV yields in MDCK cells by > 90% as compared with controls: influenza virus yield are unaffected. In BHK-21 cells, monensin also inhibits VSV production, but influenza virus is also sensitive to the ionophore. Immunofluorescent staining of fixed and unfixed MDCK monolayers indicates that VSV glycoproteins are synthesized in the presence of monensin, but their appearance on the plasma membrane is blocked. EM of VSV-infected MDCK cells treated with monensin show VSV particles aggregated within dilated cytoplasmic vesicles. Monensin-treated influenza virus-infected MDCK cells also contain dilated cytoplasmic vesicles, but virus particles were not found in these structures, and numerous influenza virions were observed budding at the cell surface. Influenza virus glycoprotein transport is apparently not blocked by monensin treatment; transport of VSV G protein is apparently blocked. A least 2 distinct pathways of transport of glycoproteins to the plasma membrane exist in MDCK cells, and 1 of them is blocked by monensin.