中国科学院分子植物科学卓越创新中心王二涛研究小组取得一项新突破。他们揭示了紫花苜蓿根瘤菌共生和免疫的激酶介质。相关论文于2025年5月6日发表在《自然》杂志上。

研究组发现了细胞质激酶MtLICK1/2，它与结瘤因子受体MtLYK3相互作用，驱动共生信号传导并抑制植物免疫。MtLICK3-1突变体的根瘤菌感染和根瘤发育存在缺陷。MtLICK1/2和MtLYK3在根瘤菌共生过程中发生相互的反式磷酸化。磷酸化的MtLYK3激活受体样激酶MtDMI2以刺激共生信号传导。MtLICK1/2在根瘤菌侵染区被激活，抑制植物免疫。它们，MtLICK1/2和MtLYK3共同放大共生信号，抑制宿主免疫，使豆科植物与根瘤菌共生。

据悉，豆科植物的根通过与土壤根瘤菌形成共生关系来保证氮的安全，但仍然对致病菌具有抵抗力。这种对根瘤菌的耐受性是如何在不损害植物免疫力的情况下实现的，在很大程度上是未知的。

附：英文原文

Title: A kinase mediator of rhizobial symbiosis and immunity in Medicago

Author: 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

Issue&Volume: 2025-05-06

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.

DOI: 10.1038/s41586-025-09057-0

Source: https://www.nature.com/articles/s41586-025-09057-0