Virus-Induced Necrosis Is a Consequence of Direct Protein-Protein Interaction between a Viral RNA-Silencing Suppressor and a Host Catalase
Virus-Induced Necrosis Is a Consequence of Direct Protein-Protein Interaction between a Viral RNA-Silencing Suppressor and a Host Catalase
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DOI：
10.1104/pp.111.180042
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发表时间：
2011-08-01
期刊：
影响因子：
7.4
通讯作者：
Masuta, Chikara
中科院分区：
文献类型：
--
作者：
Inaba, Jun-ichi;Kim, Bo Min;Masuta, Chikara
已知许多植物寄主因子在致病过程中与病毒蛋白相互作用，但植物病毒如何诱导特定的疾病症状仍需进一步研究。百合黄瓜花叶病毒株系(CMV-HL)能在侵染拟南芥的植株上诱导出离散的坏死斑，其他CMV株系也能诱导出类似的斑点，但不如CMV-HL株系明显。CMV 2b蛋白(2b)是一种已知的RNA沉默抑制因子，参与病毒运动和症状诱导。利用原位邻近连接免疫染色和原生质体分析，我们报道了CMV 2b与感染组织中的Catalase3(Cat3)直接相互作用，Cat3是分解有毒过氧化氢的关键酶。有趣的是，通常定位于细胞质(糖氧体)的Cat3通过2b和Cat3之间的相互作用被招募到细胞核。虽然在转基因植物中过表达Cat3在一定程度上减少了CMV的积累并延缓了病毒症状的发展，但2b似乎中和了参与宿主防御反应的细胞过氧化氢酶，从而有利于病毒感染。因此，我们的结果提供了证据，表明除了通过干扰microRNA途径改变症状类型外，2b还可以直接与宿主因子结合，该宿主因子在清除细胞过氧化氢方面是重要的，从而特异性地干扰该宿主因子，导致特定的坏死。
Many plant host factors are known to interact with viral proteins during pathogenesis, but how a plant virus induces a specific disease symptom still needs further research. A lily strain of Cucumber mosaic virus (CMV-HL) can induce discrete necrotic spots on infected Arabidopsis (Arabidopsis thaliana) plants; other CMV strains can induce similar spots, but they are not as distinct as those induced by CMV-HL. The CMV 2b protein (2b), a known RNA-silencing suppressor, is involved in viral movement and symptom induction. Using in situ proximity ligation assay immunostaining and the protoplast assays, we report here that CMV 2b interacts directly with Catalase3 (CAT3) in infected tissues, a key enzyme in the breakdown of toxic hydrogen peroxide. Interestingly, CAT3, normally localized in the cytoplasm (glyoxysome), was recruited to the nucleus by an interaction between 2b and CAT3. Although overexpression of CAT3 in transgenic plants decreased the accumulation of CMV and delayed viral symptom development to some extent, 2b seems to neutralize the cellular catalase contributing to the host defense response, thus favoring viral infection. Our results thus provide evidence that, in addition to altering the type of symptom by disturbing microRNA pathways, 2b can directly bind to a host factor that is important in scavenging cellular hydrogen peroxide and thus interfere specifically with that host factor, leading to the induction of a specific necrosis.