ENHANCED DISEASE RESISTANCE4 associates with CLATHRIN HEAVY CHAIN2 and modulates plant immunity by regulating relocation of EDR1 in Arabidopsis.
Obligate biotrophs, such as the powdery mildew pathogens, deliver effectors to the host cell and obtain nutrients from the infection site. The interface between the plant host and the biotrophic pathogen thus represents a major battleground for plant-pathogen interactions. Increasing evidence shows that cellular trafficking plays an important role in plant immunity. Here, we report that Arabidopsis thaliana ENHANCED DISEASE RESISTANCE4 (EDR4) plays a negative role in resistance to powdery mildew and that the enhanced disease resistance in edr4 mutants requires salicylic acid signaling. EDR4 mainly localizes to the plasma membrane and endosomal compartments. Genetic analyses show that EDR4 and EDR1 function in the same genetic pathway. EDR1 and EDR4 accumulate at the penetration site of powdery mildew infection, and EDR4 physically interacts with EDR1, recruiting EDR1 to the fungal penetration site. In addition, EDR4 interacts with CLATHRIN HEAVY CHAIN2 (CHC2), and edr4 mutants show reduced endocytosis rates. Taken together, our data indicate that EDR4 associates with CHC2 and modulates plant immunity by regulating the relocation of EDR1 in Arabidopsis.
State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
Guangheng
G
Wu
State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China University of Chinese Academy of Sciences, Beijing 100049, China.
Simu
S
Liu
State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China University of Chinese Academy of Sciences, Beijing 100049, China.
Yaofei
Y
Zhao
State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China University of Chinese Academy of Sciences, Beijing 100049, China.
Wei
W
Wang
State Key Laboratory of Plant Genomics, Institute of Microbiology, Chinese Academy of Sciences, Beijing 100101, China.
Zhaosheng
Z
Kong
State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Chinese Academy of Sciences, Beijing 100101, China dztang@genetics.ac.cn.
Dingzhong
D
Tang
D017360:Arabidopsis / Q000276:immunology* / Q000378:metabolism / Q000382:microbiology*; D029681:Arabidopsis Proteins / Q000378:metabolism*; D001203:Ascomycota / Q000502:physiology; D002462:Cell Membrane / Q000378:metabolism; D033922:Clathrin Heavy Chains / Q000378:metabolism*; D060467:Disease Resistance; D004705:Endocytosis; D011992:Endosomes / Q000378:metabolism; D016153:Genes, Suppressor; D049452:Green Fluorescent Proteins / Q000378:metabolism; D009154:Mutation / Q000235:genetics; D010935:Plant Diseases / Q000276:immunology / Q000382:microbiology; D057865:Plant Immunity; D011485:Protein Binding; D021381:Protein Transport; D020156:Salicylic Acid / Q000378:metabolism; D015398:Signal Transduction
D029681:Arabidopsis Proteins; C000606192:CHC2 protein, Arabidopsis; C423568:EDR1 protein, Arabidopsis; C000606193:EDR4 protein, Arabidopsis; D033922:Clathrin Heavy Chains; D049452:Green Fluorescent Proteins; D020156:Salicylic Acid