PaRXLR40, a broad cell death suppressor of the kauri dieback pathogen Phytophthora agathidicida, targets a plant ARM/BTB domain-containing protein

Abstract

O_LIPhytophthora agathidicida, the causal agent of kauri dieback, secretes RXLR effector proteins to promote host colonisation. One of these, PaRXLR40, was previously shown to suppress immune responses in Nicotiana benthamiana, but its mechanism of action and contribution to virulence remained unclear. C_LIO_LITo investigate PaRXLR40 function, we used comparative approaches in N. benthamiana and Agathis australis (kauri), including RNA interference (RNAi), transient expression assays, confocal microscopy, yeast two-hybrid screens, and infection assays. We also examined host protein interactors and tested mutant variants to evaluate functional domains. C_LIO_LISilencing PaRXLR40 reduced P. agathidicida colonization in N. benthamiana and A. australis. PaRXLR40 interacted with a host BTB/ARM domain protein (ARIA), previously implicated in abscisic acid (ABA) signalling. ARIA suppressed immunity and promoted infection, while interacting with NbSOG1, a DNA damage-associated transcription factor that enhanced resistance when overexpressed. External application of ABA enhanced P. agathidicida infection in both hosts, supporting the hypothesis that PaRXLR40 may hijack host ABA signalling through ARIA to promote susceptibility. C_LIO_LIOur findings show that PaRXLR40 targets ARIA to manipulate host immunity and promote virulence. The interaction between ARIA and SOG1 suggests PaRXLR40 may interfere with host transcriptional reprogramming. PaRXLR40 represents a potential target for future RNAi-based strategies to reduce kauri dieback. C_LI