To successfully invade new hosts, plant viruses must break host resistance and be competent to move within and between plant cells. As a means, viral proteins known as pathogenicity determinants have evolved to coordinate a network of protein interactions. The βC1 protein encoded by specific geminiviral satellites acts as a key pathogenicity determinant for this disease-causing family of plant viruses. Post-translational modifications (PTMs) such as ubiquitination and phosphorylation of the βC1 protein have been shown to occur in diverse viruses. However, the relevance of these and other layers of PTMs in host-geminiviral interactions has not been fully understood. Here we identified the significance of a novel layer of PTMs in the βC1 protein of Synedrella yellow vein clearing virus (SyYVCV), a newly identified member of the Begomovirus genus of Geminiviruses. This protein has conserved SUMOylation and SUMO-interacting motifs (SIMs), and we observed SUMOylation of SyYVCV βC1 in host plants as a defensive strategy against ubiquitin-mediated degradation. Counteracting this, SIMs encoded in βC1 mediate the degradation of βC1; however, both these PTMs are essential for the function of βC1 protein since SIM and SUMOylation motif mutants failed to promote pathogenicity and viral replication in vivo. SUMOylation in different motifs of βC1 led to functionally distinct outcomes, regulating the stability and function of the βC1 protein, as well as increased global SUMOylation of host proteins. Our results indicate the presence of a novel mechanism mediating a fine balance between defence and counter-defence in which a SIM site is competitively sought for degradation and, as a counter-defence, βC1 undergoes SUMOylation to escape from its degradation.

中文翻译：

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Begomoviral 致病性决定子 βC1 的稳定性通过相互拮抗的 SUMOylation 和 SIM 相互作用进行调节。


为了成功侵入新宿主，植物病毒必须打破宿主的抵抗力并能够在植物细胞内和植物细胞之间移动。作为一种手段，被称为致病性决定因素的病毒蛋白已经进化到协调蛋白质相互作用的网络。由特定双生病毒卫星编码的 βC1 蛋白是该致病植物病毒家族的关键致病性决定因素。 βC1 蛋白的泛素化和磷酸化等翻译后修饰 (PTM) 已被证明发生在多种病毒中。然而，这些和其他 PTM 层在宿主-双病毒相互作用中的相关性尚未完全了解。在这里，我们确定了 Synedrella 黄静脉清除病毒 (SyYVCV) βC1 蛋白中新的 PTM 层的重要性，SyYVCV 是双生病毒 Begomovirus 属的新发现成员。该蛋白具有保守的 SUMO 化和 SUMO 相互作用基序 (SIM)，我们在宿主植物中观察到 SyYVCV βC1 的 SUMO 化作为针对泛素介导的降解的防御策略。为了抵消这一点，βC1 中编码的 SIM 会介导 βC1 的降解；然而，这两个 PTM 对于 βC1 蛋白的功能至关重要，因为 SIM 和 SUMOylation 基序突变体未能促进体内致病性和病毒复制。 βC1 不同基序的 SUMO 化导致功能上不同的结果，调节 βC1 蛋白的稳定性和功能，并增加宿主蛋白的整体 SUMO 化。我们的结果表明存在一种介导防御和反防御之间良好平衡的新机制，其中竞争性地寻找 SIM 位点进行降解，并且作为反防御，βC1 经历 SUMOylation 以避免其降解。