Zhu Shifeng, Gao Feng, Cao Xuesong, Chen Mao, Ye Gongyin, Wei Chunhong, Li Yi
Peking-Yale Joint Center for Plant Molecular Genetics and Agrobiotechnology, National Laboratory of Protein Engineering and Plant Genetic Engineering, College of Life Science, Peking University, Beijing 100871, China.
Plant Physiol. 2005 Dec;139(4):1935-45. doi: 10.1104/pp.105.072306. Epub 2005 Nov 18.
The mechanisms of viral diseases are a major focus of biology. Despite intensive investigations, how a plant virus interacts with host factors to cause diseases remains poorly understood. The Rice dwarf virus (RDV), a member of the genus Phytoreovirus, causes dwarfed growth phenotypes in infected rice (Oryza sativa) plants. The outer capsid protein P2 is essential during RDV infection of insects and thus influences transmission of RDV by the insect vector. However, its role during RDV infection within the rice host is unknown. By yeast two-hybrid and coimmunoprecipitation assays, we report that P2 of RDV interacts with ent-kaurene oxidases, which play a key role in the biosynthesis of plant growth hormones gibberellins, in infected plants. Furthermore, the expression of ent-kaurene oxidases was reduced in the infected plants. The level of endogenous GA1 (a major active gibberellin in rice vegetative tissues) in the RDV-infected plants was lower than that in healthy plants. Exogenous application of GA3 to RDV-infected rice plants restored the normal growth phenotypes. These results provide evidence that the P2 protein of RDV interferes with the function of a cellular factor, through direct physical interactions, that is important for the biosynthesis of a growth hormone leading to symptom expression. In addition, the interaction between P2 and rice ent-kaurene oxidase-like proteins may decrease phytoalexin biosynthesis and make plants more competent for virus replication. Moreover, P2 may provide a novel tool to investigate the regulation of GA metabolism for plant growth and development.
病毒疾病的机制是生物学的一个主要研究重点。尽管进行了深入研究,但植物病毒如何与宿主因子相互作用以引发疾病仍知之甚少。水稻矮缩病毒(RDV)是植物呼肠孤病毒属的成员,可导致受感染的水稻植株出现矮化生长表型。外衣壳蛋白P2在RDV感染昆虫的过程中至关重要,因此会影响昆虫介体对RDV的传播。然而,其在水稻宿主内RDV感染过程中的作用尚不清楚。通过酵母双杂交和免疫共沉淀分析,我们发现RDV的P2蛋白在受感染植物中与贝壳杉烯氧化酶相互作用,贝壳杉烯氧化酶在植物生长激素赤霉素的生物合成中起关键作用。此外,受感染植物中贝壳杉烯氧化酶的表达降低。RDV感染植物中内源性GA1(水稻营养组织中的一种主要活性赤霉素)的水平低于健康植物。向RDV感染的水稻植株外源施用GA3可恢复正常生长表型。这些结果表明,RDV的P2蛋白通过直接的物理相互作用干扰了一种细胞因子的功能,该细胞因子对导致症状表达的生长激素的生物合成很重要。此外,P2与水稻贝壳杉烯氧化酶样蛋白之间的相互作用可能会减少植物抗毒素的生物合成,使植物更有利于病毒复制。此外,P2可能为研究植物生长发育过程中GA代谢的调控提供一种新工具。