Interaction between Cucumber mosaic virus 2b protein and plant catalase induces a specific necrosis in association with proteasome activity.
Interaction between Cucumber mosaic virus 2b protein and plant catalase induces a specific necrosis in association with proteasome activity.
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DOI：
10.1007/s00299-016-2055-2
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发表时间：
2017-01
影响因子：
6.2
通讯作者：
Masuta C
中科院分区：
文献类型：
--
作者：
Murota K;Shimura H;Takeshita M;Masuta C
黄瓜花叶病毒（CMV）可通过CMV 2b蛋白与宿主过氧化氢酶之间的相互作用诱导拟南芥特异性坏死，其中泛素-蛋白酶体途径可能参与其中。 我们之前报道过，CMV 2b 蛋白（病毒 RNA 沉默抑制子）与 H2O2 清除剂过氧化氢酶（CAT3）相互作用，导致接种 CMV 的拟南芥叶片坏死。我们在此证实，CMV 在 CAT3 敲除突变体（cat3）中可以更丰富地积累，并且 CAT3 使宿主植物对 CMV 的耐受性更强。我们还发现，坏死的严重程度并不能简单地用CAT3缺乏所产生的高水平H2O2来解释，因为重组CMV，CMV-N，在cat3中诱导的坏死比野生型中温和得多，这表明了坏死诱导的一些特定机制。为了进一步表征与 CAT3 结合相关的 2b 诱导坏死，我们进行了农杆菌渗透实验，以在本塞姆氏烟草叶子中过表达 CAT3 和 2b。 CAT3 与 CMV-N 2b (N2b) 共表达时的积累水平高于与 CMV-Y 2b (Y2b) 共表达时的积累水平。我们推断 N2b 与 CAT3 形成的复合物比 Y2b 更稳定，并且 2b-CAT3 复合物的寿命似乎对于诱导坏死很重要。通过使用抗泛素抗体进行免疫沉淀 (IP)，然后使用抗 CAT3 抗体进行检测，我们在 IP 蛋白中检测到了较高分子量的涂片和 CAT3 的几种分解产物。此外，蛋白酶体抑制剂MG132治疗实际上可以增加CAT3的积累水平。这项研究表明，宿主蛋白酶体途径至少部分负责 CAT3 的降解，这在 CMV 感染的组织中表现出来。本文的在线版本 (doi:10.1007/s00299-016-2055-2) 包含补充材料，可供授权用户使用。
Cucumber mosaic virus (CMV) can induce a specific necrosis on Arabidopsis through the interaction between the CMV 2b protein and host catalase, in which the ubiquitin–proteasome pathway may be involved. We previously reported that the CMV 2b protein, the viral RNA silencing suppressor, interacted with the H2O2 scavenger catalase (CAT3), leading to necrosis on CMV-inoculated Arabidopsis leaves. We here confirmed that CMV could more abundantly accumulate in the CAT3-knockout mutant (cat3), and that CAT3 makes host plants a little more tolerant to CMV. We also found that the necrosis severity is not simply explained by a high level of H2O2 given by the lack of CAT3, because the recombinant CMV, CMV-N, induced much milder necrosis in cat3 than in the wild type, suggesting some specific mechanism for the necrosis induction. To further characterize the 2b-inducing necrosis in relation to its binding to CAT3, we conducted the agroinfiltration experiments to overexpress CAT3 and 2b in N. benthamiana leaves. The accumulation levels of CAT3 were higher when co-expressed with the CMV-N 2b (N2b) than with CMV-Y 2b (Y2b). We infer that N2b made a more stable complex with CAT3 than Y2b did, and the longevity of the 2b–CAT3 complex seemed to be important to induce necrosis. By immunoprecipitation (IP) with an anti-ubiquitin antibody followed by the detection with anti-CAT3 antibodies, we detected a higher molecular-weight smear and several breakdown products of CAT3 among the IP-proteins. In addition, the proteasome inhibitor MG132 treatment could actually increase the accumulation levels of CAT3. This study suggests that the host proteasome pathway is, at least partially, responsible for the degradation of CAT3, which is manifested in CMV-infected tissues. The online version of this article (doi:10.1007/s00299-016-2055-2) contains supplementary material, which is available to authorized users.
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