1 2 Plant parasites must colonise and reproduce on plants to survive. In most cases, active immune 3 responses, triggered by (conserved) microbe-encoded molecules keep invaders at bay. Post-4 translational modifications (PTMs) of proteins are vital for contextual regulation and integration of 5 plant immune responses. Pathogens and pests secrete proteins (effectors) to interfere with plant 6 immunity through modification of host target functions and disruption of immune signalling 7 networks. Importantly, molecular virulence strategies of distinct pathogens converge on a small 8 set of regulators with central roles in plant immunity. The extent of convergence between pathogen 9and herbivorous insect virulence strategies is largely unexplored. Here we report that effectors 10 from the oomycete pathogen, Phytophthora capsici, and the major aphid pest, Myzus persicae 11 target the host immune regulator SIZ1, an E3 SUMO ligase. SIZ1-regulated immunity in 12 Arabidopsis against bacterial pathogens is known to require the resistance protein SNC1, and 13 signalling components PAD4 and EDS1. We show that SIZ1 functions as a negative regulator of 14 plant immunity to aphids and an oomycete pathogen. However, this immune regulation is 15 independent of SNC1, PAD4 and EDS1-signalling pointing to the presence of a novel SIZ1-16 mediated immune signalling route. Our results suggest convergence of distinct pathogen and pest 17 virulence strategies on an E3 SUMO ligase that negatively regulates plant immunity.
19Introduction 20 The plant immune system is complex, featuring different classes of receptors to detect pathogens 21 and pests and initiate a multi-layered defence responses. Pattern recognition receptors (PRRs) 22 recognize conserved pest and pathogen molecules, called pathogen associated molecular patterns 23 (PAMPs), to activate immune responses and fight off the intruder (Jones and Dangl, 2006; 24 Monaghan and Zipfel, 2012). Pathogens and pests deliver an arsenal of effector proteins inside 25 their host to counter these and other plant defence pathways to promote effector-triggered 26 susceptibility (ETS) through modulation of host protein activities. In addition, these effectors likely 27 contribute to effective infection or infestation strategies by promoting the release of nutrients to 28 support pathogen or pest growth. Another layer of plant immunity may be activated upon 29 recognition of these effectors, or their activities, by nucleotide-binding leucine-rich repeat proteins 30 (NLRs), which usually is associated with the activation of a Hypersensitive Response (HR). Given 31 that plants carefully balance energy allocation between growth, development and reproduction, 32 any effective immune responses need to be appropriate and controlled (Huot et al., 2014).
34The identification of effector host targets and their effector-induced modification(s) can reveal the 35 mechanistic basis of virulence and the biological processes that lead to susceptibility. Moreover, 36 the identification of effector host target...