Glycine‐serine‐rich effector PstGSRE4 in Puccinia striiformis f. sp. tritici targets and stabilizes TaGAPDH2 that promotes stripe rust disease

Abstract Puccinia striiformis f. sp. tritici ( Pst ) secretes effector proteins that enter plant cells and manipulate host processes. In a previous study, we identified a glycine‐serine‐rich effector PstGSRE4, which was proven to regulate the reactive oxygen species (ROS) pathway by interacting with TaCZSOD2. In this study, we further demonstrated that PstGSRE4 interacts with wheat glyceraldehyde‐3‐phosphate dehydrogenase TaGAPDH2, which is related to ROS signalling. In wheat, silencing of TaGAPDH2 by virus‐induced gene silencing increased the accumulation of ROS induced by the Pst virulent race CYR31. Overexpression of TaGAPDH2 decreased the accumulation of ROS induced by the avirulent Pst race CYR23. In addition, TaGAPDH2 suppressed Pst candidate elicitor Pst322‐triggered cell death by decreasing ROS accumulation in Nicotiana benthamiana . Knocking down TaGAPDH2 expression attenuated Pst infection, whereas overexpression of TaGAPDH2 promoted Pst infection, indicating that TaGAPDH2 is a negative regulator of plant defence. In N. benthamiana , PstGSRE4 stabilized TaGAPDH2 through inhibition of the 26S proteasome‐mediated destabilization. Overall, these results suggest that TaGAPDH2 is hijacked by the Pst effector as a negative regulator of plant immunity to promote Pst infection in wheat.