Dimerization and proper degradation of Bombyx mori nucleopolyhedorivirus IE2 are required for efficient virus growth in B. mori larvae

Dimerization and proper degradation of Bombyx mori nucleopolyhedorivirus IE2 are required for efficient virus growth in B. mori larvae
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家蚕核多角体病毒 IE2 的二聚化和适当降解是病毒在家蚕幼虫中有效生长所必需的

DOI:
10.1007/s13355-012-0159-x
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发表时间:
2013
影响因子:
1.3
通讯作者:
and Katsuma S
and Katsuma S
中科院分区:
农林科学3区
文献类型:
--
作者:
Tsuchida A;Ishihara G;Shimada T;and Katsuma S

文献摘要

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杆状病毒2基因是直接早期基因之一,已知其产物可反式激活病毒启动子。然而,家蚕核型多角体病毒(BmNPV)ie2在昆虫幼虫中的作用尚不清楚。在这里,我们研究了BmNPV IE2在培养细胞和昆虫幼虫中的功能,使用两种突变病毒,BmIE2D和BmIE2CS。BmIE2D缺乏IE2二聚化所需的IE2 C末端卷曲螺旋结构域。另一个突变体BmIE2CS表达E3连接酶活性缺陷型IE2衍生物,其与野生型IE2相比降解更慢。我们发现,这2个突变对BmNPV感染培养细胞的影响很小,而在B.桑天牛感染162株突变体。这些结果表明,BmNPV IE2的二聚化和适当的降解是病毒在B.在培养的细胞中没有。经口感染试验也表明,封闭型的fie2突变体在B中的感染性是正常的。与报道的苜蓿银纹夜蛾核型多角体病毒20个突变体的结果不一致。这表明IE2功能的丧失导致宿主昆虫中的病毒特异性效应。
The baculovirusie2gene is one of the immediate early genes, and its product is known to transactivate viral promoters. However, the roles ofBombyx morinucleopolyhedrovirus (BmNPV)ie2in insect larvae are poorly understood. Here we investigated the functions of BmNPV IE2 in cultured cells and in insect larvae using two mutant viruses, BmIE2D and BmIE2CS. BmIE2D lacks the IE2 C-terminal coiled-coil domain that is required for IE2 dimerization. The other mutant BmIE2CS expresses an E3 ligase activity-deficient IE2 derivative, which is degraded more slowly compared with wild-type IE2. We found thatie2mutations had little effect on BmNPV infection in cultured cells, whereas budded virus and occlusion body production was significantly reduced in the hemolymph ofB. morilarvae infected withie2mutants. These results indicate that both dimerization and proper degradation of BmNPV IE2 are crucial steps for efficient virus growth inB. morilarvae, but not in cultured cells. Oral infection assays also revealed that the infectivity of the occluded form ofie2mutants was normal inB. morilarvae, which is inconsistent with the results reported fromie2mutants ofAutographa californicaNPV. This suggests that loss of IE2 function causes virus-specific effects in host insects.