Plasmopara viticola effector PvRXLR131 suppresses plant immunity by targeting plant receptor‐like kinase inhibitor BKI1

Abstract

Summary The grapevine downy mildew pathogen Plasmopara viticola secretes a set of RXLR effectors (PvRXLRs) to overcome host immunity and facilitate infection, but how these effectors function is unclear. Here, the biological function of PvRXLR131 was investigated via heterologous expression. Constitutive expression of PvRXLR131 in Colletotrichum gloeosporioides significantly enhanced its pathogenicity on grapevine leaves. Constitutive expression of PvRXLR131 in Arabidopsis promoted Pseudomonas syringae DC3000 and P. syringae DC3000 (hrcC‐) growth as well as suppressed defence‐related callose deposition. Transient expression of PvRXLR131 in Nicotiana benthamiana leaves could also suppress different elicitor‐triggered cell death and inhibit plant resistance to Phytophthora capsici. Further analysis revealed that PvRXLR131 interacted with host Vitis vinifera BRI1 kinase inhibitor 1 (VvBKI1), and its homologues in N. benthamiana (NbBKI1) and Arabidopsis (AtBKI1). Moreover, bimolecular fluorescence complementation analysis revealed that PvRXLR131 interacted with VvBKI1 in the plasma membrane. Deletion assays showed that the C‐terminus of PvRXLR131 was responsible for the interaction and mutation assays showed that phosphorylation of a conserved tyrosine residue in BKI1s disrupted the interaction. BKI1 was a receptor inhibitor of growth‐ and defence‐related brassinosteroid (BR) and ERECTA (ER) signalling. When silencing of NbBKI1 in N. benthamiana, the virulence function of PvRXLR131 was eliminated, demonstrating that the effector activity is mediated by BKI1. Moreover, PvRXLR131‐transgenic plants displayed BKI1‐overexpression dwarf phenotypes and suppressed BR and ER signalling. These physiological and genetic data clearly demonstrate that BKI1 is a virulence target of PvRXLR131. We propose that P. viticola secretes PvRXLR131 to target BKI1 as a strategy for promoting infection.

A novel effector CfEC92 of Colletotrichum fructicola contributes to glomerella leaf spot virulence by suppressing plant defences at the early infection phase

“…, 2017; Lan et al . , 2019). Because CfEC92 functions in host cells, our next work will focus on seeking the possible targets of CfEC92 in apple leaf cells in order to elucidate the molecular basis underlying plant defence suppression.…”

Plasmopara viticola effector PvRXLR111 stabilizes VvWRKY40 to promote virulence

“…In our previous studies, 83 PvRXLR effectors, cloned from a Chinese P. viticola isolate, were characterized based on subcellular location and the ability to suppress cell death induced by two elicitors, INF1 and Bax (Liu et al, 2018). Many PvRXLR effectors were found to be able to suppress plant immunity, and of these PvRXLR131 was further shown to suppress plant immunity by targeting BKI1 (Lan et al, 2019). Meanwhile, several PvRXLRs were shown to induce cell death when expressed in Nicotiana benthamiana (Liu et al, 2018).…”

Plasmopara viticola effector PvRXLR159 suppresses immune responses in Nicotiana benthamiana

“…Infection of P. viticola 'JL-7-2ʹ was performed according to previous studies. 20,24 The susceptible grapevine (V. vinifera 'Thompson Seedless') leaf discs were inoculated with 30 µL spore suspension with a final concentration of 1 × 10 5 spores/mL on the abaxial side, and then incubated in an incubator (18ºC, 11 h light/13 h dark, 66% relative humidity). Phenotypic monitoring and sampling for RNA extraction were performed at indicated times.…”

“…23 Our recent studies revealed that PvRXLR131 suppresses host resistance by targeting BRI1 kinase inhibitor 1. 24 In this study, we characterized the role of PvRXLR159 in plant-microbe interaction.…”