青枯菌
生物
胡椒粉
免疫
青枯病
基因沉默
基因
微生物学
植物免疫
获得性免疫系统
细胞生物学
免疫系统
效应器
寄主(生物学)
病毒学
细胞分裂素
病菌
先天免疫系统
毒力
遗传学
作者
Qiaoling Lu,Yu Huang,Meiyun Wan,Jingang Lv,Xingge Cheng,Yutong Zheng,官德义,Sheng Yang,Shuilin He
摘要
Abstract It has been previously found that pepper (Capsicum annuum) activates high-temperature specific immunity against R. solanacearum in cytokinin signalling dependent manner at high temperature (37°C), while how this high-temperature specific immunity is activated remain unclear. Herein, we demonstrate that both CaARR2 and CaLBD24 acted positively in pepper immunity against R. solanacearum infection at 37°C but not at 28°C. CaLBD24 was found to interact in the nuclei with CaARR2, which is otherwise present in plastids upon R. solanacearum infection at 28°C but translocated into the nuclei upon 37°C exposure alone, R. solanacearum infection at 37°C or the exogenous application of ABA or R. solanacearum infection at 28°C combined with exogenous application of tZ. By ChIP-seq combined with RNA-seq assay, the CaARR2-CaLBD24 module in the nuclei was further found to activate high temperature specific immunity by directly co-targeting and activating genes including CaRPT2 via binding their corresponding cis-elements, and CaRPT2 was further found by virus gene silencing to act positively in pepper immunity against R. solanacearum at 37°C. In addition, CaARR2, CaLBD24 and CaRPT2 ware also found to act positively in defense response of tomato R. solanacearum infection at 37°C. The results uncover that high-temperature specific immunity is activated in pepper and tomato in cytokinin signalling dependent manner using ARR2-LBD24 module to activate genes including RPT2, providing new insights into mechanism underlying bacterial wilt resistance in pepper and tomato at high temperatures.
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