Abstract
Downy mildew is one of the most serious diseases of grapevine (Vitis spp). The causal agent of grapevine downy mildew, Plasmopara viticola, is an obligate biotrophic oomycete. Although oomycete pathogens such as P. viticola are known to secrete RxLR effectors to manipulate host immunity, there have been few studies of the associated mechanisms by which these may act. Here, we show that a candidate P. viticola RxLR effector, PvAvh74, induces cell death in Nicotiana benthamiana leaves. Using agroinfiltration, we found that nuclear localization, two putative N-glycosylation sites, and 427 amino acids of the PvAvh74 carboxyl terminus were necessary for cell-death-inducing activity. Using virus-induced gene silencing (VIGS), we found that PvAvh74-induced cell death in N. benthamiana requires EDS1, NDR1, SGT1, RAR1, and HSP90, but not BAK1. The MAPK cascade components MEK2, WIPK, and SIPK were also involved in PvAvh74-induced cell death in N. benthamiana. Transient expression of PvAvh74 could suppress Phytophthora capsici colonization of N. benthamiana, which suggests that PvAvh74 elicits plant immune responses. Suppression of P. capsici colonization also was dependent on nuclear localization of PvAvh74. Additionally, PvAvh74-triggered cell death could be suppressed by another effector, PvAvh8, from the same isolate. This work provides a framework to further investigate the interactions of PvAvh74 and other RxLR effectors with host immunity.
Highlights
Plants are subject to attack by various pathogens, and to prevent pathogen invasion, they have developed a two-tier, innate immune system (Jones and Dangl, 2006)
Expression of PvAvh74 caused necrosis in N. tabacum, but not in grape in vitro (V. vinifera susceptible cultivar Thomson seedless) (Supplementary Figure S3). These results indicated that PvAvh74 can induce cell death in N. benthamiana and N. tabacum leaves
PvAvh74-induced cell death was observed in BAK1/SERK3 silenced plants (Figure 5A). These results indicated that cell death triggered by PvAvh74 in N. benthamiana leaves depends on SGT1, Hsp90, RAR1, EDS1, and NDR1, but not BAK1
Summary
Plants are subject to attack by various pathogens, and to prevent pathogen invasion, they have developed a two-tier, innate immune system (Jones and Dangl, 2006). The first-tier immunity is activated by pattern recognition receptors (PRRs), which recognize specific molecules secreted by the pathogen. Such molecules are termed pathogen/microbe-associated molecular patterns (PAMP/MAMPs), and include fungal chitin and bacterial flagellin at the plasma membrane (Nürnberger et al, 2004; Bittel and Robatzek, 2007; Naito et al, 2008). This recognition is a basal immune mechanism and is termed PAMP-triggered immunity, or PTI (Jones and Dangl, 2006). Second-tier immunity is related to resistance proteins, encoded by R genes, which recognize the
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