Role and Mechanism of Suppressed Apoplastic Serine Hydrolase Activities during Infection with Pseudomonas syringae

• Applicant: Professor Dr. Renier A.L. van der Hoorn
• Subject Area: Plant Biochemistry and Biophysics ; Plant Genetics and Genomics
• Term: from 2013 to 2015
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 245104334

The extracellular space surrounding plant cells (the apoplast) is arguably the largest biotic interface on earth. This surface is humid and rich in nutrients and consequently many microbes, mostly commensal and pathogenic bacteria, have adapted to thrive in this environment. The apoplast is also littered with hydrolytic plant enzymes and even more are secreted during immune responses triggered upon microbial infection. These apoplastic hydrolases are thought to degrade microbial components and release elicitors that trigger immunity. The emerging picture is that microbes are able to manipulate the apoplast to suppress these host enzyme activities. However, to what extend this occurs and how and why is still poorly understood. Our preliminary data demonstrates that the activities of secreted plant serine hydrolases are suppressed during infection of Nicotiana benthamiana with Pseudomonas syringe by secreted inhibitors. Interestingly, surveys of apoplastic proteomes revealed the accumulation of a plant-encoded Kunitz inhibitor in the apoplast of infected plants, leading to the intriguing hypothesis that Pseudomonas purposefully induces apoplastic Kunitz levels in the host to suppress hydrolase activities in the apoplast. This proposal is aimed at confirming this hypothesis and revealing the biological relevance of the suppressed hydrolase activities and elucidating the deeper underlying molecular mechanisms. We will use integrated approaches involving targeted gene silencing, complementation with synthetic (mutant) genes, activity profiling, and pathogen assays.

• DFG Programme: Research Grants