Several vector-borne plant pathogens have evolved mechanisms to exploit and to hijack vector host cellular, molecular, and defense mechanisms for their transmission. In the past few years, Liberibacter species, which are transmitted by several psyllid vectors, have become an economically important group of pathogens that have devastated the citrus industry and caused tremendous losses to many other important crops worldwide. The molecular mechanisms underlying the interactions of Liberibacter species with their psyllid vectors are poorly studied. “Candidatus Liberibacter solanacearum,” which is associated with important vegetable diseases, is transmitted by the carrot psyllid Bactericera trigonica in a persistent manner. Here, we elucidated the role of the B. trigonica Arp2/3 protein complex, which plays a major role in regulation of the actin cytoskeleton, in the transmission of “Ca. Liberibacter solanacearum.” “Ca. Liberibacter solanacearum” colocalized with ArpC2, a key protein in this complex, and this colocalization was strongly associated with actin filaments. Silencing of the psyllid ArpC2 disrupted the colocalization and the dynamics of F-actin. Silencing of RhoGAP21 and Cdc42, which act in the signaling cascade leading to upregulation of Arp2/3 and F-actin bundling, showed similar results. On the other hand, silencing of ArpC5, another component of the complex, did not induce any significant effects on F-actin formation. Finally, ArpC2 silencing caused a 73.4% reduction in “Ca. Liberibacter solanacearum” transmission by psyllids, strongly suggesting that transmission of “Ca. Liberibacter solanacearum” by B. trigonica is cytoskeleton dependent and “Ca. Liberibacter solanacearum” interacts with ArpC2 to exploit the intracellular actin nucleation process for transmission. Targeting this unique interaction could lead to the development of a novel strategy for the management of Liberibacter-associated diseases.

中文翻译：

---

肌动蛋白细胞骨架介导胡萝卜木虱传播“ Candidatus Liberibacter solanacearum”。

几种媒介传播的植物病原体已发展出利用和劫持媒介宿主细胞，分子和防御机制进行传播的机制。在过去的几年中，Liberibacter物质，其在几个木虱媒介传播，已经成为破坏该柑橘产业，并造成了巨大的损失，许多其他重要的全球作物病原体一种重要的经济团体。利比里亚细菌物种与它们的木耳载体相互作用的分子机制研究很少。与重要的植物病有关的“ Candidatus Liberibacter solanacearum”通过胡萝卜木虱Bactericera trigonica传播坚持不懈地 在这里，我们阐明了B. trigonica Arp2 / 3蛋白复合物在Ca的传播中的作用，该复合物在肌动蛋白细胞骨架的调节中起主要作用。青枯菌。” “钙。“青枯细菌”与该复合物中的关键蛋白ArpC2共定位，并且该共定位与肌动蛋白丝紧密相关。木虱ArpC2的沉默破坏了共定位和F-肌动蛋白的动力学。RhoGAP21和Cdc42沉默，在信号级联反应中导致Arp2 / 3和F-肌动蛋白捆绑的上调，表现出相似的结果。另一方面，沉默复合物的另一个成分ArpC5，对F-肌动蛋白的形成没有明显的影响。最后，ArpC2沉默导致“ Ca ”降低73.4％。Liberibacter菌”由木虱传输，强烈暗示的发送“的Ca。Trigonica B. trigonica的“ Liberibacter solanacearum”具有细胞骨架依赖性，“钙。Solanacearum细菌”与ArpC2相互作用，以利用细胞内肌动蛋白成核过程进行传播。针对这种独特的相互作用可能导致开发一种新的策略来管理与利比里亚细菌相关的疾病。