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A lesion‐mimic mutant was obtained from a mutagenic treatment performed with ethyl methanesulfonate on the Argentine bread wheat ( Triticum aestivum ) cultivar Sinvalocho M.A. The HLP (hypersensitive‐like phenotype) mutant exhibited tiny, discrete, white lesions in the absence of any pathogen, resembling the typical hypersensitive response (HR). The lesions only became evident once the fifth or sixth leaf emerged, and spread at random along the leaf blades and leaf sheaths of the developing plant, including tissues of the spike. Because the lesion‐mimic mutant showed no lesions at the seedling stage, the phenotypes of both the mutant and its mother line were identical at this point. Histochemical studies showed that spontaneous hypersensitive‐like lesions in the HLP mutant corresponded to cell death. In leaf‐rust ( Puccinia triticina ) infection experiments performed at seedling and adult‐plant stages, adult HLP plants showed enhanced resistance to leaf‐rust attack compared with plants of Sinvalocho M.A. of comparable developmental stage, suggesting that the HLP mutation may confer increased resistance to the fungus. Because enhanced resistance coincided with the presence of spontaneous HR lesions, activation of HLP plant defence responses appeared to be tightly linked to this phenomenon. Final plant height and yield components in the lesion‐mimic mutant did not differ from those of the mother line, indicating that the HLP mutation caused no detrimental pleiotropic effects that significantly affected agronomic performance. These data support the direct use of mutations in disease‐resistance breeding.