TheRalstonia pseudosolanacearumeffector RipE1 is recognized at the plasma membrane byNbPtr1, Nicotiana benthamianahomolog ofPseudomonas tomato race 1

AbstractThe bacterial wilt disease caused by soil-borne bacteria of theRalstonia solanacearumspecies complex (RSSC) threatens important crops worldwide. Only a few immune receptors conferring resistance to this devastating disease are known so far. Individual RSSC strains deliver around 70 different type III secretion system effectors into host cells to manipulate the plant physiology and dampen immune responses. RipE1 is an effector conserved across RSSC isolated from diverse plant species and triggers immune responses in the model SolanaceaeNicotiana benthamiana. Here, we used multiplexed virus-induced gene silencing of the nucleotide-binding and leucine-rich repeat receptor family to identify the genetic basis of RipE1 recognition inN. benthamiana. Specific silencing of theN. benthamianahomolog ofSolanum lycopersicoides Pseudomonas tomato race 1gene (NbPtr1) completely abolished RipE1-induced hypersensitive response and immunity toRalstonia pseudosolanacearum. In Nb-ptr1knock-out plants, expression of the nativeNbPtr1coding sequence was sufficient to restore RipE1 recognition. In addition to the putative catalytic triad Cys-His-Asp, RipE1 association with the host cell plasma membrane was found necessary for NbPtr1-dependent recognition. Furthermore, we found that NbPtr1-dependent recognition of RipE1 natural variants is polymorphic suggesting the coevolutionary nature of this interaction. This work hence provides an additional evidence for the indirect mode of activation of NbPtr1 and supports NbPtr1 relevance for resistance to bacterial wilt disease in Solanaceae.