Wheat powdery mildew is a significant threat to wheat production, necessitating the development of disease-resistant varieties as an economically viable and environmentally sustainable strategy. In this study, we investigated a semi-dominant mutant, necrosis leaf (necl), which exhibits spontaneous necrotic lesions and enhanced resistance to powdery mildew. We identified that the necl phenotype is caused by a Lys-to-Glu gain-of-function mutation at position 421 in the coiled-coil nucleotide-binding leucine-rich repeat (CC-NLR) protein TaCNL, through the combination of map-based cloning, transformation, and mutagenesis. Further analysis indicated that the TaCNL mutant enhanced resistance to powdery mildew likely through activation of the phenylalanine catabolic process and increased salicylic acid levels. Importantly, artificially modifying the amino acid at position 421 of TaCNL to an acidic residue induces immune necrosis, suggesting a potential strategy for engineering disease-resistant proteins. These findings provide novel insights into the dual role of TaCNL in modulating growth and defence in wheat and offer a valuable genetic resource for developing durable resistance in wheat.