PhD Exit Seminar – Derek Seto (Desveaux Lab)

Recognition of the Pseudomonas syringae type III effector HopF1r by the Arabidopsis NLR ZAR1

Abstract

The plant pathogen Pseudomonas syringae uses the needle-like type III secretion system (T3SS) to inject virulence factors known as type III secreted effector proteins (T3SEs) directly into the plant cell. T3SEs disrupt plant immune pathways, allowing for successful colonization. However, plants have evolved resistance (R) genes that encode for nucleotide-binding leucine-rich repeat (NLR) proteins that detect the presence of some effectors, and subsequently trigger an immune response that suppresses pathogen growth. Recognition of effectors by NLRs often involves monitoring another host protein for effector-induced molecular perturbations; upon detection of these modifications, an immune response is triggered. For example, the NLR ZAR1 senses effector-mediated perturbations of associated kinases to detect at least 6 families of T3SEs. The effector HopF2a/HopF1r from P. syringae pv. aceris M302273PT has been found to trigger immunity in Arabidopsis. The objective of my research was 1) to identify other potential genetic requirements for HopF2a/HopF1r recognition in Arabidopsis, and 2) to understand how these components are involved in the HopF2a/HopF1r recognition mechanism. In this thesis, I demonstrate that recognition of HopF2a/HopF1r requires the R gene ZAR1, as well as the kinases ZRK3 and PBL27. The results of this project provide insight into how a single NLR is able to recognize several unrelated effectors by associating with different members of a diverse family of kinases, providing plants with the potential to defend themselves against a wide variety of pathogens.

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Join Zoom Meeting

https://utoronto.zoom.us/j/87272098970

Meeting ID: 872 7209 8970

Host: Darrell Desveaux (darrell.desveaux@utoronto.ca)

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