A hypermorphic allele of CNGC confers broad-spectrum blast resistance through ectopic calcium influx-induced cell death in rice.

Rice blast, caused by Magnaporthe oryzae, is one of the most destructive diseases threatening global rice production. Race-independent broad-spectrum resistance (BSR) holds the ideal strategy for durable rice blast management, yet its molecular mechanisms remain largely obscure. Here, we identified and characterized elicitor-triggered cell death 1 (etd1), a rice lesion mimic mutant that displays spontaneous cell death and hypersensitive response (HR)-like necrosis upon challenge with M. oryzae elicitors. Genetic analysis reveals that etd1 encodes a hypermorphic haplotype of rice Cyclic Nucleotide-Gated Channel 13 (OsCNGC13) protein, harboring a single glycine-to-glutamic acid substitution (G483E) in the highly conserved gating domain of the CNGC family. This mutation transforms OsCNGC13 into a hyperactive Ca2+-permeable channel (etd1), driving ectopic Ca2+ influx under both developmental and pathogenic conditions that lead to cell death. Although detrimental to agronomic traits, etd1 confers robust BSR against all 108 tested M. oryzae isolates by effectively blocking fungal colonization through ectopic Ca2+ influx-induced cell death. Our data demonstrate that hyperactivation of a Ca2+-permeable channel can confer rice BSR through Ca2+-mediated cell death. The discovery of etd1 provides a valuable clue for breeding rice with broad-spectrum blast resistance based on Ca2+-permeable channels.