A Novel Set of SNARE Partners Facilitating Bacterial Pathogen Defence

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Plant microbial pathogens destroy some 15% of crop production worldwide, inflicting major agricultural and socio-economic losses. Thus, understanding plant immunity is at the centre of efforts to mitigate the challenges in food production facing human society in the coming decades. Although plants have evolved defence systems, immunity comes at a cost to plant growth; crop bred to maximize growth-related traits, by contrast, often compromise on defense. To strategically maximize plant disease resistance, knowledge of the mechanisms underlying plant defences is vital to minimize reductions in yield. Stomatal pores on the leaf surface exchange gas and water with the environment and are primary entry points for microbial pathogen. The initial defence against bacterial pathogen is stomatal closure, but pathogens commonly manipulate these defences and force stomatal opening. At a cellular level, these manipulations include commandeering ion transporters and their regulatory proteins to prevent stomata closure. Microbial pathogens also hijack cellular vesicle traffic to suppress secretion of defence-related molecules to the cell wall. Secretion at the plant plasma membrane is mediated by so-called SNARE proteins that assemble to drive the final stages of membrane vesicle fusion and deliver the vesicle contents to the cell wall and space outside the cell. Yet, the knowledge of molecular basis of these processes during plant pathogenesis is sparse and virtually nothing is known of their coordination. The plasma membrane SNARE SYP132 has been associated with the secretion of antimicrobial peptides. Recently, I found that its expression and traffic within the cell are tied directly to bacterial infection. SYP132 expression, I observed, affects stomatal responses to bacterial pathogens. Furthermore, SYP132 interacts physically with the plasma membrane ion transporters and regulatory proteins that are essential for pathogen defence, and traffic of the SNARE appears to co-opt the ion transport proteins during pathogen infection. These findings point to an unexpected and central role for this SNARE as a key regulator of in stomatal defence and immunity. My hypothesis is that SYP132 endocytosis and vesicle membrane recycling are critical for early stages of bacterial pathogenesis. SYP132 traffic and functions in immunity are particularly regulated by its interactions with the ion transporters and regulatory proteins at the plasma membrane and they allow for a co-ordination between defence signalling, antimicrobial secretion and stomatal responses to fight off disease and to regulate plant-microbe interactions. I propose to elucidate the mechanisms underlying SYP132 traffic and its impact on the transporter binding partners to resolve the impact on plant immunity. These studies will make use of established plant and pathogen models as a backdrop for the work. I will determine how interactions of SYP132, particularly with the ion transporter and regulatory proteins identified to date, change during the progression of bacterial disease. I will expand the studies with proteomic analysis of the SYP132 interactome and measurement of quantitative changes in SYP132 interactions with new and known partners during bacterial pathogenesis to assess their roles in SYP132-mediated immunity. The knowledge gained will inform future efforts in approaches to engineering crops with enhanced defence systems in sustainable agriculture.