Effector FpECIR from Fusarium pseudograminearum targets wheat ethylene signaling pathway to suppress plant immunity

Fusarium pseudograminearum (F. pseudograminearum) is the main causal agent of Fusarium Crown Rot (FCR) posing a severe threat to wheat yield. Effectors, as one class of weapons of phytopathogens, help pathogens infect their hosts by disturbing plant immunity. In this study, we identified a secreted effector, FpECIR, which has no functional domains, suppresses INF1-triggered cell death in Nicotiana benthamiana. Once translocated into wheat cells, FpECIR (without signal peptide) interacts with TaPLATZ2B, and silencing TaPLATZ2B and its alleles makes wheat more susceptible to F. pseudograminearum. Deletion of residues 29-35 of FpECIR disrupted its interaction with TaPLATZ2B, and eliminated its ability to suppress INF1-induced cell death. The pathogenicity of deletion mutants ΔFpecir on wheat coleoptiles was significantly reduced. Analysis of transcriptome data showed that infection with the ΔFpecir strain triggered the upregulation of defense-related genes in wheat coleoptiles, many of which were functionally enriched in hormone signaling pathways. qRT-PCR results revealed that FpECIR suppressed the expression of TaPLATZ2B and of genes related to ethylene signaling pathway. Furthermore, EMSA experiment result proved that FpECIR can inhibit the ability of TaPLATZ2B binding with the promoter region of ethylene response factors (TaERF020L). Suppressing the transcription levels of genes related to ethylene biosynthesis made the wheats more susceptible to FCR. Overall, the results showed that FpECIR plays an important role in the pathogenicity of F. pseudograminearum, and that the integrity of FpECIR is necessary for its interaction with TaPLATZ2B and for its suppression of INF1-induced cell death. Additionally, FpECIR not only affects the expression of TaPLATZ2B but also inhibits the function of TaPLATZ2B to regulate plant defense response through ethylene signaling pathways.