AUTOGRAPHA-CALIFORNICA-M NUCLEAR POLYHEDROSIS-VIRUS - MICROTUBULES AND REPLICATION
AUTOGRAPHA-CALIFORNICA-M NUCLEAR POLYHEDROSIS-VIRUS - MICROTUBULES AND REPLICATION
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DOI：
10.1016/0042-6822(90)90211-9
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发表时间：
1990-03-01
期刊：
影响因子：
3.7
通讯作者：
ZAAL, KJM
中科院分区：
文献类型：
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作者：
VOLKMAN, LE;ZAAL, KJM
微管的渐进重组和解聚与病毒诱导的苜蓿银纹夜蛾M核多角体病毒（AcMNPV）感染的草地贪夜蛾IPLB-Sf-21细胞的变圆相对应，表明微管有助于维持这些细胞的正常形状。秋水仙碱对所有皮质和大部分核旁微管的解聚也导致细胞变圆，证实了这一假设。对阿非迪霉素和放线菌酮的研究表明，病毒对微管的诱导作用是由早期和晚期病毒基因产物介导的。感染 p10 缺失突变体的细胞中的微管以与野生型病毒感染的细胞中类似的方式解聚微管，表明 p10 与病毒诱导的微管变化无关。尽管如此，p10 和微管关联的证据是通过荧光显微镜和免疫电子显微镜获得的。 感染前和感染过程中秋水仙碱对微管的解聚不会干扰病毒复制，但用紫杉醇（一种微管稳定剂）处理细胞，既延迟又抑制了病毒复制。添加秋水仙碱可以减轻紫杉醇诱导的作用。这些结果表明，AcMNPV 诱导的微管解聚可能是病毒复制的必要事件，而不是病毒复制的切向效应。由于中间丝蛋白抗体和 IPLB-Sf-21 细胞之间缺乏交叉反应性，监测病毒感染对中间丝的影响的尝试没有成功，这表明这些蛋白在鳞翅目昆虫细胞中并不高度保守。
Progressive reorganization and depolymerization of microtubules corresponded with virus-induced rounding of Autographa californica M nuclear polyhedrosis virus (AcMNPV)-infected Spodoptera frugiperda IPLB-Sf-21 cells, suggesting that microtubules were instrumental in maintaining the normal shape of these cells. Depolymerization of all cortical and most of the paranuclear microtubules with colchicine also resulted in cell rounding confirming this hypothesis. Studies with aphidicolin and cycloheximide indicated the virus-induced effects on the microtubules were mediated by both early and late viral gene products. Microtubules in cells infected with a p10 deletion mutant depolymerized microtubules in a manner similar to those in wild-type virus-infected cells, indicating p10 was not responsible for virus-induced changes in the microtubules. Nevertheless, evidence for the association of p10 and microtubules was obtained by fluorescence microscopy and immunoelectron microscopy. Colchicine depolymerization of microtubules before and throughout infection did not interfere with virus replication, but treatment of cells with taxol, a microtubule-stabilizing agent, both delayed and depressed virus replication. The taxol-induced effect was relieved by the addition of colchicine. These results suggested that AcMNPV-induced depolymerization of microtubules may be a necessary event in, rather than a tangential effect of, virus replication. Attempts to monitor the effects of virus infection on intermediate filaments were unsuccessful due to the lack of cross-reactivity between antibodies to intermediate filament proteins and IPLB-Sf-21 cells, indicating these proteins are not highly conserved in lepidopteran insect cells.