A hypermorphic allele of CNGC confers broad‐spectrum blast resistance through ectopic calcium influx‐induced cell death in rice
Jianbin Liu, Gui Xiao, Hai Liu, Yi Liang, Zhaofeng Yi, Bin Bai, Xiushuo Liang, Sheng Luo, Fang Yuan, Jie Yang, Shaowu Xue, Wenxian Sun, Bo Zhou, Jun WuSummary
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 Ca
2+
‐permeable channel (etd1), driving ectopic Ca
2+
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 Ca
2+
influx‐induced cell death.
Our data demonstrate that hyperactivation of a Ca
2+
‐permeable channel can confer rice BSR through Ca
2+
‐mediated cell death. The discovery of
etd1
provides a valuable clue for breeding rice with broad‐spectrum blast resistance based on Ca
2+
‐permeable channels.