Wang Dapeng, Jin Rui, Shi Xiaobao, Guo Haoran, Tan Xinhang, Zhao Achen, Lian Xinghua, Dai Huiling, Li Shaozhuang, Xin Kexu, Tian Changfu, Yang Jun, Chen Wansheng, Macho Alberto P, Wang Ertao
New Cornerstone Science Laboratory, Key Laboratory of Plant Carbon Capture, CAS Center for Excellence in Molecular Plant Sciences, Institute of Plant Physiology and Ecology, Chinese Academy of Sciences, Shanghai, China.
The SATCM Key Laboratory for New Resources and Quality Evaluation of Chinese Medicine, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai, China.
Nature. 2025 May 6. doi: 10.1038/s41586-025-09057-0.
Legume roots secure nitrogen by forming a symbiosis with soil rhizobia but remain resistant to pathogenic bacteria. 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 signalling 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 transphosphorylation during rhizobial symbiosis. Phosphorylated MtLYK3 activates the receptor-like kinase MtDMI2 to stimulate symbiotic signalling. MtLICK1/2 is activated in the rhizobial infection area to suppress plant immunity. Thus, MtLICK1/2 and MtLYK3 together amplify symbiotic signalling and dampen host immunity to enable legume-rhizobium symbiosis.
豆科植物的根通过与土壤根瘤菌形成共生关系来固定氮,但对病原菌仍具有抗性。在不损害植物免疫的情况下如何实现这种对根瘤菌的耐受性,目前尚不清楚。在这里,我们鉴定出细胞质激酶MtLICK1/2,它与结瘤因子受体MtLYK3相互作用,以驱动共生信号传导并抑制植物免疫。在Mtlick1/2中,根瘤菌感染和根瘤发育存在缺陷,这与Mtlyk3-1突变体的表型相似。在根瘤菌共生过程中,MtLICK1/2和MtLYK3进行相互转磷酸化。磷酸化的MtLYK3激活类受体激酶MtDMI2以刺激共生信号传导。MtLICK1/2在根瘤菌感染区域被激活以抑制植物免疫。因此,MtLICK1/2和MtLYK3共同放大共生信号并减弱宿主免疫,从而实现豆科植物与根瘤菌的共生。