Glycine maxNNL1 restricts symbiotic compatibility with widely distributed bradyrhizobia via root hair infection
文献类型： 外文期刊
作者： Zhang, Bao 1 ; Wang, Mengdi 1 ; Sun, Yifang 3 ; Zhao, Peng 3 ; Liu, Chang 1 ; Qing, Ke 1 ; Hu, Xiaotong 1 ; Zhong, Zhedon 1 ;
作者机构： 1.Huazhong Agr Univ, Coll Life Sci & Technol, Ctr Integrat Biol, Wuhan, Peoples R China
2.Henan Univ, State Key Lab Crop Stress Adaptat & Improvement, Kaifeng, Peoples R China
3.Huazhong Agr Univ, Coll Life Sci & Technol, State Key Lab Agr Microbiol, Wuhan, Peoples R China
4.Hebei Acad Agr & Forestry Sci, Inst Cereal & Oil Crops, Hebei Lab Crop Genet & Breeding, Shijiazhuang, Hebei, Peoples R China
5.ARS, Soybean Genom & Improvement Lab, USDA, Beltsville, MD USA
期刊名称：NATURE PLANTS （ 影响因子：15.793； 五年影响因子：17.349 ）
ISSN： 2055-026X
年卷期： 2021 年 7 卷 1 期
页码：
收录情况： SCI
摘要： Symbiosis between soybean (Glycine max) and rhizobia is essential for efficient nitrogen fixation. Rhizobial effectors secreted through the type-III secretion system are key for mediating the interactions between plants and rhizobia, but the molecular mechanism remains largely unknown. Here, our genome-wide association study for nodule number identified G. maxNodule Number Locus 1 (GmNNL1), which encodes a new R protein. GmNNL1 directly interacts with the nodulation outer protein P (NopP) effector from Bradyrhizobium USDA110 to trigger immunity and inhibit nodulation through root hair infection. The insertion of a 179 bp short interspersed nuclear element (SINE)-like transposon into GmNNL1 leads to the loss of function of GmNNL1, enabling bradyrhizobia to successfully nodulate soybeans through the root hair infection route and enhancing nitrogen fixation. Our findings provide important insights into the coevolution of soybean-bradyrhizobia compatibility and offer a way to design new legume-rhizobia interactions for efficient symbiotic nitrogen fixation. Soybean accessions display a variable number of nodules when colonized by rhizobia. The authors identify one locus controlling this trait, a typical TIR-NBS-LRR disease resistance gene called NNL1, and the corresponding bacterial effector called NopP.
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