A novel non-canonical rectifying calcium channel in rice triggers cell death mediated robust immunity

Wu, Jun, Jianbin Liu, Gui Xiao, Hai Liu, Yi Liang, Zhaofeng Yi, Bai Bin et al. "A Novel Non-Canonical Rectifying Calcium Channel in Rice Triggers Cell Death Mediated Robust Immunity." Pre-print.

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.