Shuang Zhang, Lingzhi Meng, Zhichao Zhao, Changyan Qi, Chen Xie, Xiaokang Jiang, Ling Jiang, Yulong Ren, Zhijun Cheng, Jie Wang, Qibing Lin, Xiuping Guo, Xin Wang, Shanshan Zhu, Cailin Lei, Jianmin Wan

Plant Physiology; 2026; IF: 8.2

DOI:10.1093/plphys/kiag663

Abstract

Programmed cell death and immunity in plants are finely orchestrated to promote antimicrobial defense while preventing autoimmunity. However, the molecular mechanisms involved are not fully understood. Here, we isolated a rice mutant ecdr1 (enhanced cell death and resistance 1) that displayed an autoimmunity phenotype and enhanced resistance to rice blast and bacterial blight, and identified ECDR1 as a new shared component in PI3K and PI4K complexes, linking the hyccin-containing protein with plant defense responses. ECDR1 was expressed at all developmental stages and in all tissues examined. The ECDR1 was highly conserved in function across monocots and dicots. The 113 bp deletion in the ECDR1 promoter reduced its expression, leading to cell death and enhanced disease resistance. The ECDR1 was localized in plasma membrane, and interacted with TPR1 and TPR2 which in turn interacted with both PI4K1 and PI3K1, suggesting that ECDR1 could function as a component associated with not only PI4K complexes but also PI3K complexes to help catalyze PI into PI3P and PI4P. The lethality of all homozygous ecdr1, pi3k1 and tpr1 tpr2 mutants indicated the crucial roles of these genes in plant normal growth, which restricted our understanding of PI3K and PI4K functions. Alternatively, exogenous application of PI3K and PI4K inhibitors could substantially exacerbate the cell death and enhance disease resistance, implying their roles in plant immunity. Our findings provide novel insights into the regulatory mechanisms of ECDR1 in cell death and defense pathways, will aid in understanding the functions of PI3K and PI4K in plant immunity.