| Sumario: | Plants utilize calcium as a signaling molecule to regulate innate immunity, including PAMP-triggered immunity (PTI) and effector-triggered immunity (ETI), in addition to controlling growth and development1,2. Recent extensive research has highlighted that the activation of calcium ion (Ca2+) channels during PTI and the formation of Ca2+ channels during ETI are crucial for plant immunity3. However, comprehension on how crops substantially augment immunity through the enhancement of Ca2+ channel activity remains limited. Here, we report a rice lesion mimic mutant, called etd1 (elicitors triggered cell death 1), which also triggers cell death formation upon the challenge of rice blast elicitors. The recessive gain-of-function gene etd1 encodes a hypermorphic haplotype of OsCNGC13 which contains a single amino acid substitution of glycine-to-glutamate at the position of 483rd amino acid. The etd1 forms a novel non-canonical rectifying Ca2+ channel that significantly enhances Ca2+ influx. We position that etd1-driven excessive Ca2+ influx disrupts cellular calcium homeostasis, thereby triggering pathogen-induced cell death and conferring robust and broad-spectrum immunity to the rice blast pathogen.
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