Instituto de Hortofruticultura Subtropical y Mediterranea, Universidad de Málaga-Consejo Superior de Investigaciones Científicas, Departamento de Biología Celular y Genética, Universidad de Málaga, Campus de Teatinos, E-29071 Malaga, Spain.
Plant Cell. 2011 Mar;23(3):1014-32. doi: 10.1105/tpc.110.080267. Epub 2011 Mar 25.
Viruses must create a suitable cell environment and elude defense mechanisms, which likely involves interactions with host proteins and subsequent interference with or usurpation of cellular machinery. Here, we describe a novel strategy used by plant DNA viruses (Geminiviruses) to redirect ubiquitination by interfering with the activity of the CSN (COP9 signalosome) complex. We show that geminiviral C2 protein interacts with CSN5, and its expression in transgenic plants compromises CSN activity on CUL1. Several responses regulated by the CUL1-based SCF ubiquitin E3 ligases (including responses to jasmonates, auxins, gibberellins, ethylene, and abscisic acid) are altered in these plants. Impairment of SCF function is confirmed by stabilization of yellow fluorescent protein-GAI, a substrate of the SCF(SLY1). Transcriptomic analysis of these transgenic plants highlights the response to jasmonates as the main SCF-dependent process affected by C2. Exogenous jasmonate treatment of Arabidopsis thaliana plants disrupts geminivirus infection, suggesting that the suppression of the jasmonate response might be crucial for infection. Our findings suggest that C2 affects the activity of SCFs, most likely through interference with the CSN. As SCFs are key regulators of many cellular processes, the capability of viruses to selectively interfere with or hijack the activity of these complexes might define a novel and powerful strategy in viral infections.
病毒必须创造一个适宜的细胞环境并逃避防御机制,这可能涉及与宿主蛋白的相互作用,以及随后对细胞机制的干扰或篡夺。在这里,我们描述了一种植物 DNA 病毒(双生病毒)用于通过干扰 CSN(COP9 信号体)复合物的活性来重新定向泛素化的新策略。我们表明,双生病毒 C2 蛋白与 CSN5 相互作用,其在转基因植物中的表达会损害 CUL1 上的 CSN 活性。几种由 CUL1 为基础的 SCF 泛素 E3 连接酶(包括对茉莉酸、生长素、赤霉素、乙烯和脱落酸的反应)调控的反应在这些植物中发生改变。通过稳定 SCF(SLY1)的底物黄色荧光蛋白-GAI,证实了 SCF 功能的损伤。这些转基因植物的转录组分析突出了对茉莉酸的反应是受 C2 影响的主要 SCF 依赖过程。拟南芥的外源茉莉酸处理破坏了双生病毒的感染,表明抑制茉莉酸反应可能对感染至关重要。我们的发现表明,C2 影响 SCF 的活性,很可能是通过干扰 CSN。由于 SCF 是许多细胞过程的关键调节剂,病毒选择性干扰或劫持这些复合物活性的能力可能定义了病毒感染的一种新的强大策略。