Abstract
The RxLR effector family, produced by oomycete pathogens, may manipulate host physiological and biochemical events inside host cells. A group of putative RxLR effectors from Plasmopara viticola have been recently identified by RNA-Seq analysis in our lab. However, their roles in pathogenesis are poorly understood. In this study, we attempted to characterize 23 PvRxLR effector candidates identified from a P. viticola isolate “ZJ-1-1.” During host infection stages, expression patterns of the effector genes were varied and could be categorized into four different groups. By using transient expression assays in Nicotiana benthamiana, we found that 17 of these effector candidates fully suppressed programmed cell death elicited by a range of cell death-inducing proteins, including BAX, INF1, PsCRN63, PsojNIP, PvRxLR16 and R3a/Avr3a. We also discovered that all these PvRxLRs could target the plant cell nucleus, except for PvRxLR55 that localized to the membrane. Furthermore, we identified a single effector, PvRxLR28, that showed the highest expression level at 6 hpi. Functional analysis revealed that PvRxLR28 could significantly enhance susceptibilities of grapevine and tobacco to pathogens. These results suggest that most P. viticola effectors tested in this study may act as broad suppressors of cell death to manipulate immunity in plant.
Highlights
During co-evolution with microbial pathogens, plants have evolved multiple layers of innate immune surveillance that successful pathogens have evolved to evade or suppress
When the transcriptional levels of effector genes were measured at different time courses during the infection (0, 6, 12, 24, 48, 72, 96, and 120 hpi), all the 23 PvRxLR genes identified from the P. viticola strain “ZJ-1-1” were up-regulated at some time points
A similar pattern of induction was described for RxLR effectors of H. arabidopsidis and P. sojae which has been termed “immediate-early, low” (Wang et al, 2011; Anderson et al, 2012)
Summary
During co-evolution with microbial pathogens, plants have evolved multiple layers of innate immune surveillance that successful pathogens have evolved to evade or suppress. The first layer is comprised of pattern recognition receptors (PRRs) that recognize broadly conserved pathogen molecules (pathogen/microbe-associated molecular patterns, PAMP/MAMPs), and activate defense responses including the induction of defense genes, production of reactive oxygen species (ROS) and deposition of callose (Jones and Dangl, 2006). This recognition leads to the so-called PAMP (or pattern)- triggered immunity (PTI; Katagiri and Tsuda, 2010). Successful pathogens can deliver effectors into plant cell to suppress or interfere with PTI, resulting in effector-triggered susceptibility. A hallmark of this recognition is the programmed cell death (PCD), termed hypersensitive response (HR) which
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