Biology subjects

Segonzac, C.

Publications and source records attributed to Segonzac, C..

3 recordsLinked to original sources

bioRxiv2023

The Ralstonia pseudosolanacearum effector RipE1 is recognized at the plasma membrane by NbPtr1, Nicotiana benthamiana homolog of Pseudomonas tomato race 1.

The bacterial wilt disease caused by soil-borne bacteria of the Ralstonia solanacearum species 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 Solanaceae Nicotiana 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 in N. benthamiana. Specific silencing of the N. benthamiana homolog of Solanum lycopersicoides Pseudomonas tomato race 1 gene (NbPtr1) completely abolished RipE1-induced hypersensitive response and immunity to Ralstonia pseudosolanacearum. In Nb-ptr1 knock-out plants, expression of the native NbPtr1 coding 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.

plant biology↗

bioRxiv2022

Ptr1 and ZAR1 immune receptors confer overlapping and distinct bacterial pathogen effector specificities

Nucleotide-binding and leucine-rich repeat receptors (NLRs) detect pathogen effectors inside the plant cell. To identify Nicotiana benthamiana NLRs (NbNLRs) with novel effector recognition specificity, we designed an NbNLR VIGS library and conducted a rapid reverse genetic screen. During the NbNLR VIGS library screening, we identified that N. benthamiana homolog of Ptr1 (PSEUDOMONAS SYRINGAE PV. TOMATO RACE 1 RESISTANCE) recognizes the Pseudomonas effectors AvrRpt2, AvrRpm1, and AvrB. We demonstrated that recognition of the Xanthomonas effector AvrBsT and the Pseudomonas effector HopZ5 in N. benthamiana is conferred independently by N. benthamiana homolog of Ptr1 and ZAR1 (HOPZ-ACTIVATED RESISTANCE 1). In addition, we showed that the RLCK XII family protein JIM2 (XOPJ4 IMMUNITY 2) physically interacts with AvrBsT and HopZ5 and is required for the NbZAR1-dependent recognition of AvrBsT and HopZ5. The recognition of multiple bacterial effectors by Ptr1 and ZAR1 in N. benthamiana demonstrates a convergent evolution of effector recognition across plant species. Identification of key components involved in Ptr1 and ZAR1 mediated immunity would reveal unique mechanisms of expanded effector recognition and be useful for engineering resistance in solanaceous crops.

plant biology↗

bioRxiv2022

The Phytophthora capsici RxLR effector CRISIS2 has roles in suppression of PTI and triggering cell death in host plant

Pathogen effectors can suppress various plant immune responses, suggesting that they have multiple targets in the host. To understand the mechanisms underlying plasma membrane-associated and effector-mediated immunity, we performed Phytophthora capsici RxLR cell death Inducer Suppressing Immune System (CRISIS) screening. In Nicotiana benthamiana, the cell death induced by the RxLR effector CRISIS2 is inhibited by the irreversible plasma membrane H+-ATPase (PMA) activator fusicoccin. Biochemical and gene silencing analyses revealed that CRISIS2 physically and functionally associates with PMAs and induces host cell death independent of immune receptors. CRISIS2 induces apoplastic alkalization by suppressing PMA activity via its association with the C-terminal regulatory domain of PMA. In planta expression of CRISIS2 significantly enhanced the virulence of P. capsici, whereas host-induced gene silencing of CRISIS2 compromised disease symptom and biomass of P. capsici. Furthermore, co-immunoprecipitation assays revealed that CRISIS2 constitutively associates with BAK1, the co-receptor of pattern recognition receptors (PRRs). CRISIS2 interferes with the FLS2-BAK1 complex induced by flagellin perception and impairs downstream signaling from the PRR complex. Proteomics and gene silencing assays identified putative PRRs that negatively regulate the virulence of P. capsici in N. benthamiana as interactors of CRISIS2 and BAK1. Our study identified a novel RxLR effector playing multiple roles in the suppression of plant defense and induction of cell death to support the pathogen hemibiotrophic life cycle in the host plant.

plant biology↗