Several vector-borne plant pathogens have evolved mechanisms to exploit and hijack vector host cellular, molecular and defense mechanisms for their transmission. Over the past few years, Liberibacter species, which are transmitted by several psyllid vectors, have become an economically important group of pathogens that 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 (CLso) associated with important vegetable diseases is transmitted by the carrot psyllid, Bactericera trigonica in a persistent manner. Here, we elucidated the role of B. trigonica Arp2/3 protein complex, which plays a major role in the regulation of the actin cytoskeleton, in the transmission of CLso. CLso co-localized with ArpC2, a key protein in this complex, and this co-localization strongly associated with actin filaments. Silencing the psyllid ArpC2 disrupted the co-localization and the dynamics of F-actin. Silencing RhoGAP21 and Cdc42, which act in the signaling cascade leading to upregulation of Arp2/3 and F-actin bundling, also showed similar results. On the other hand, silencing ArpC5, another component of the complex, did not induce any significant effects on F-actin formation. Finally, ArpC2 silencing caused 73.4% reduction in CLso transmission by psyllids, strongly suggesting that its transmission by B. trigonica is cytoskeleton-dependent and it interacts with ArpC2 to exploit the intracellular actin nucleation process for transmission. Targeting this unique interaction could lead to developing a novel strategy for the management of Liberibacter-associated diseases.
IMPORTANCE Plant diseases caused by vector-borne pathogens are responsible for tremendous losses and threaten some of the most important agricultural crops. A good example is the citrus greening disease caused by bacteria of the genus Liberibacter and transmitted by psyllids, and has devastated the citrus industry in the US, China and Brazil. Here we show that the psyllid-transmitted Candidatus Liberibacter solanacearum (CLso) employs the actin cytoskeleton of psyllid gut cells, specifically the ArpC2 protein in the Arp2/3 complex of this system, for movement and transmission in the vector. Silencing ArpC2 dramatically influenced interaction of CLso with the cytoskeleton and decreased the bacteria transmission to plants. This system could be targeted for developing a novel approach for the control of Liberibacter- associated diseases.