The Arabidopsis Cucumovirus Multiplication 1 and 2 Loci Encode Translation Initiation Factors 4E and 4G

The Arabidopsis Cucumovirus Multiplication 1 and 2 Loci Encode Translation Initiation Factors 4E and 4G
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DOI:
10.1128/jvi.78.12.6102-6111.2004
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发表时间:
2004-06
影响因子:
5.4
通讯作者:
Motoyasu Yoshii;M. Nishikiori;K. Tomita;Norimichi Yoshioka;R. Kozuka;S. Naito;M. Ishikawa
Motoyasu Yoshii;M. Nishikiori;K. Tomita;Norimichi Yoshioka;R. Kozuka;S. Naito;M. Ishikawa
中科院分区:
医学2区
文献类型:
--
作者:
Motoyasu Yoshii;M. Nishikiori;K. Tomita;Norimichi Yoshioka;R. Kozuka;S. Naito;M. Ishikawa

文献摘要

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摘要拟南芥的Cum1和Cum2突变抑制了黄瓜花叶病毒(CMV)的增殖。在Cum1和Cum2原生质体中,CMV RNA和外壳蛋白的积累达到野生型水平,但CMV细胞间移动所必需的3a蛋白的积累明显低于野生型原生质体。在Cum2原生质体中,芜菁皱缩病毒(TCV)相关RNA和蛋白质的积累也减少了。定位克隆证实了CUM1和CUM2分别编码真核翻译起始因子4E和4G。与大多数细胞RNA不同,CMV RNA没有Poly(A)尾,而TCV RNA既没有5‘末端帽,也没有Poly(A)尾。利用携带CMV或TCV RNA末端结构和未翻译序列的嵌合荧光素酶mRNA进行体内翻译分析,证明这些病毒未翻译序列含有正向或负向调节编码蛋白表达的元件。Cum1和Cum2突变对这些元件的作用有不同的影响,表明Cum1和Cum2突变导致CMV 3a蛋白的低效产生,而Cum2突变影响TCV编码蛋白的产生。
ABSTRACT The cum1 and cum2 mutations of Arabidopsis thaliana inhibit cucumber mosaic virus (CMV) multiplication. In cum1 and cum2 protoplasts, CMV RNA and the coat protein accumulated to wild-type levels, but the accumulation of the 3a protein of CMV, which is necessary for cell-to-cell movement of the virus, was strongly reduced compared with that in wild-type protoplasts. In cum2 protoplasts, the accumulation of turnip crinkle virus (TCV)-related RNA and proteins was also reduced. Positional cloning demonstrated that CUM1 and CUM2 encode eukaryotic translation initiation factors 4E and 4G, respectively. Unlike most cellular mRNA, the CMV RNA lacks a poly(A) tail, whereas the TCV RNA lacks both a 5′-terminal cap and a poly(A) tail. In vivo translation analyses, using chimeric luciferase mRNA carrying the terminal structures and untranslated sequences of the CMV or TCV RNA, demonstrated that these viral untranslated sequences contain elements that regulate the expression of encoded proteins positively or negatively. The cum1 and cum2 mutations had different effects on the action of these elements, suggesting that the cum1 and cum2 mutations cause inefficient production of CMV 3a protein and that the cum2 mutation affects the production of TCV-encoded proteins.