Durable rust resistance in wheat conferred by engineering host protein TaHRLI to evade recognition by the virulence effector PstCRT.
Guo, Shuangyuan; Zhang, Yanqin; Zhang, Xinmei; Du, Xiaoya; Zhang, Feng; Li, Huankun; Wang, Xiaojie; Kang, Zhensheng; Zhang, Xinmei
Current biology
DOI：10.1016/j.cub.2026.01.001
Abstract
Endoplasmic reticulum (ER) stress and the hypersensitive response (HR) are recognized as cornerstones of plant immunity; however, the mechanistic synergy and the strategies pathogens employ to dismantle this alliance remain elusive. Here, we identify a virulence effector, PstCRT (calreticulin), from Puccinia striiformis f. sp. tritici (Pst), that suppresses host immune responses by disrupting ER stress-mediated HR. PstCRT directly targets the HR-like lesion-inducing protein (TaHRLI) in wheat and obstructs its ER translocation. Within the ER lumen, TaHRLI interacts with wheat calreticulin (TaCRT), triggering Ca⁺ efflux and activating the unfolded protein response (UPR) to induce cell death and disease resistance. Pathogen-derived PstCRT structurally mimics TaCRT to sequester TaHRLI to the plasma membrane via competitive interaction, thereby effectively suppressing ER stress-induced HR initiation. Crucially, we found that CRT secretion represents a conserved virulence strategy across different rust genera. AlphaFold-guided engineering of TaHRLI in wheat generated the TaHRLIMut variant that evades PstCRT recognition. Overexpressing TaHRLIMut in wheat conferred broad-spectrum resistance against Pst in biennial field trials, effectively mitigating pathogen-induced yield losses while preserving essential agronomic traits. Collectively, this study elucidates a molecular mechanism underlying pathogen disruption of ER stress-induced HR to promote infection and proposes an innovative strategy for engineering durable crop protection.