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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通过相互拮抗的SUMOylation和SIM相互作用，可调节前乳腺病原性决定因素βC1的稳定性。

为了成功入侵新宿主，植物病毒必须打破宿主抗性，并具有在植物细胞内和植物细胞之间移动的能力。作为一种手段，被称为致病性决定簇的病毒蛋白质已经进化为协调蛋白质相互作用网络的工具。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。已显示翻译后修饰（PTM）（例如βC1蛋白的泛素化和磷酸化）在多种病毒中发生。但是，还没有完全了解PTM的这些层和其他层与宿主-双病毒相互作用中的相关性。在这里，我们确定了Synedrella黄色静脉清洁病毒（SyYVCV）的βC1蛋白中新的PTM层的重要性，新鉴定出的双子病毒的双歧杆菌属成员。该蛋白质具有保守的SUMOylation和与SUMO相互作用的基序（SIMs），并且我们观察到宿主植物中SyYVCVβC1的SUMOylation是针对泛素介导的降解的防御策略。与此相反，以βC1编码的SIM介导了βC1的降解。然而，由于SIM和SUMOylation基序突变体不能促进体内的致病性和病毒复制，因此这两个PTM对βC1蛋白的功能都是必不可少的。βC1的不同基序中的SUMOylation导致功能上不同的结果，调节βC1蛋白的稳定性和功能，以及宿主蛋白的整体SUMOylation增加。