AP2 transcription factors play a crucial role in plant development and reproductive growth, as well as response to biotic and abiotic stress. However, the role of TaAP2-15, in the interaction between wheat and the stripe fungus, Puccinia striiformis f. sp. tritici (Pst), remains elusive. In this study, we isolated TaAP2-15 and characterized its function during the interaction. TaAP2-15 was localized in the nucleus of wheat and N. benthamiana. Silencing of TaAP2-15 by barley stripe mosaic virus (BSMV)-mediated VIGS (virus-induced gene silencing) increased the susceptibility of wheat to Pst accompanied by enhanced growth of the pathogen (number of haustoria, haustorial mother cells and hyphal length). We confirmed by quantitative real-time PCR that the transcript levels of pathogenesis-related genes (TaPR1 and TaPR2) were down-regulated, while reactive oxygen species (ROS)-scavenging genes (TaCAT3 andTaFSOD3D) were induced accompanied by reduced accumulation of H2O2. Furthermore, we found that TaAP2-15 interacted with a zinc finger protein (TaRZFP34) that is a homolog of OsRZFP34 in rice. Together our findings demonstrate that TaAP2-15 is positively involved in resistance of wheat to the stripe rust fungus and provides new insights into the roles of AP2 in the host-pathogen interaction.

A biotrophic fungus, Puccinia striiformis f.sp. tritici (Pst), which causes stripe rust disease in wheat is the most yield-limiting factor in wheat production. Plants have complex defense mechanisms against invading pathogens. Hypersensitive response (HR), a kind of programmed cell death (PCD) at the infection site, is among these defense mechanisms. Transcription factors (TFs) play a crucial role in plant defense response against invading pathogens. Myeloblastosis (MYB) TFs are among the largest TFs families that are involved in response to both biotic and abiotic stresses. However, little is known about the mechanisms of MYB TFs during the interaction between wheat and the stripe rust fungus. Here, we identified an R2R3 MYB TF from wheat, designated as TaMYB391, and characterized its functional role during wheat–Pst interaction. Our data indicated that TaMYB391 is induced by Pst infection and exogenous application of salicylic acid (SA) and abscisic acid (ABA). TaMYB391 is localized in the nucleus of both wheat and Nicotiana benthamiana. Transient overexpression of TaMYB391 in N. benthamiana triggered HR-related PCD accompanied by increased electrolyte leakage, high accumulation of reactive oxygen species (ROS), and transcriptional accumulation of SA defense-related genes and HR-specific marker genes. Overexpression of TaMYB391 in wheat significantly enhanced wheat resistance to stripe rust fungus through the induction of pathogenesis-related (PR) genes, ROS accumulation and hypersensitive cell death. On the other hand, RNAi-mediated silencing of TaMYB391 decreased the resistance of wheat to Pst accompanied by enhanced growth of the pathogen. Together our findings demonstrate that TaMYB391 acts as a positive regulator of HR-associated cell death and positively contributes to the resistance of wheat to the stripe rust fungus by regulating certain PR genes, possibly through SA signaling pathways.