Dapeng Wang,Rui Jin,Xiaobao Shi,Haoran Guo,Xinhang Tan,Achen Zhao,Xinghua Lian,Huiling Dai,Shaozhuang Li,Kexu Xin,Changfu Tian,Jun Yang,Wansheng Chen,Alberto P Macho,Ertao Wang
{"title":"A kinase mediator of rhizobial symbiosis and immunity in Medicago.","authors":"Dapeng Wang,Rui Jin,Xiaobao Shi,Haoran Guo,Xinhang Tan,Achen Zhao,Xinghua Lian,Huiling Dai,Shaozhuang Li,Kexu Xin,Changfu Tian,Jun Yang,Wansheng Chen,Alberto P Macho,Ertao Wang","doi":"10.1038/s41586-025-09057-0","DOIUrl":null,"url":null,"abstract":"Legume roots secure nitrogen by forming a symbiosis with soil rhizobia but remain resistant to pathogenic bacteria1-4. How this tolerance to rhizobia is achieved without compromising plant immunity is largely unknown. Here, we identify the cytoplasmic kinase MtLICK1/2, which interacts with nodulation factor receptor MtLYK3 to drive symbiotic signaling and suppress plant immunity. Rhizobial infection and nodule development are defective in Mtlick1/2, phenocopying the Mtlyk3-1 mutant. MtLICK1/2 and MtLYK3 undergo reciprocal trans-phosphorylation during rhizobial symbiosis. Phosphorylated MtLYK3 activates the receptor-like kinase MtDMI2 to stimulate symbiotic signaling. MtLICK1/2 is activated in the rhizobia infection area to suppress plant immunity. Thus, MtLICK1/2 and MtLYK3 together amplify symbiotic signaling and dampen host immunity to enable legume-rhizobium symbiosis.","PeriodicalId":18787,"journal":{"name":"Nature","volume":"47 1","pages":""},"PeriodicalIF":50.5000,"publicationDate":"2025-05-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Nature","FirstCategoryId":"103","ListUrlMain":"https://doi.org/10.1038/s41586-025-09057-0","RegionNum":1,"RegionCategory":"综合性期刊","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q1","JCRName":"MULTIDISCIPLINARY SCIENCES","Score":null,"Total":0}
引用次数: 0
Abstract
Legume roots secure nitrogen by forming a symbiosis with soil rhizobia but remain resistant to pathogenic bacteria1-4. How this tolerance to rhizobia is achieved without compromising plant immunity is largely unknown. Here, we identify the cytoplasmic kinase MtLICK1/2, which interacts with nodulation factor receptor MtLYK3 to drive symbiotic signaling and suppress plant immunity. Rhizobial infection and nodule development are defective in Mtlick1/2, phenocopying the Mtlyk3-1 mutant. MtLICK1/2 and MtLYK3 undergo reciprocal trans-phosphorylation during rhizobial symbiosis. Phosphorylated MtLYK3 activates the receptor-like kinase MtDMI2 to stimulate symbiotic signaling. MtLICK1/2 is activated in the rhizobia infection area to suppress plant immunity. Thus, MtLICK1/2 and MtLYK3 together amplify symbiotic signaling and dampen host immunity to enable legume-rhizobium symbiosis.
期刊介绍:
Nature is a prestigious international journal that publishes peer-reviewed research in various scientific and technological fields. The selection of articles is based on criteria such as originality, importance, interdisciplinary relevance, timeliness, accessibility, elegance, and surprising conclusions. In addition to showcasing significant scientific advances, Nature delivers rapid, authoritative, insightful news, and interpretation of current and upcoming trends impacting science, scientists, and the broader public. The journal serves a dual purpose: firstly, to promptly share noteworthy scientific advances and foster discussions among scientists, and secondly, to ensure the swift dissemination of scientific results globally, emphasizing their significance for knowledge, culture, and daily life.