Bao Hanbin, Wang Yanan, Li Haoxing, Wang Qiang, Lei Yutao, Ye Ying, Wadood Syed F, Zhu Hui, Staehelin Christian, Stacey Gary, Xu Shutong, Cao Yangrong
National Key Lab of Agricultural Microbiology, Hubei Hongshan Laboratory, Huazhong Agricultural University, Wuhan, China.
State Key Laboratory of Biocontrol and Guangdong Key Laboratory of Plant Resources, School of Life Sciences, Sun Yat-sen University, Guangzhou, China.
Elife. 2025 Apr 4;13:RP97196. doi: 10.7554/eLife.97196.
It is well documented that type-III effectors are required by Gram-negative pathogens to directly target different host cellular pathways to promote bacterial infection. However, in the context of legume-rhizobium symbiosis, the role of rhizobial effectors in regulating plant symbiotic pathways remains largely unexplored. Here, we show that NopT, a YopT-type cysteine protease of NGR234 directly targets the plant's symbiotic signaling pathway by associating with two Nod factor receptors (NFR1 and NFR5 of ). NopT inhibits cell death triggered by co-expression of NFR1/NFR5 in . Full-length NopT physically interacts with NFR1 and NFR5. NopT proteolytically cleaves NFR5 both in vitro and in vivo, but can be inactivated by NFR1 as a result of phosphorylation. NopT plays an essential role in mediating rhizobial infection in . Autocleaved NopT retains the ability to cleave NFR5 but no longer interacts with NFR1. Interestingly, genomes of certain species only harbor genes encoding truncated proteins without the autocleavage site. These results reveal an intricate interplay between rhizobia and legumes, in which a rhizobial effector protease targets NFR5 to suppress symbiotic signaling. NFR1 appears to counteract this process by phosphorylating the effector. This discovery highlights the role of a bacterial effector in regulating a signaling pathway in plants and opens up the perspective of developing kinase-interacting proteases to fine-tune cellular signaling processes in general.
有充分的文献记载，革兰氏阴性病原体需要III型效应蛋白直接靶向不同的宿主细胞途径以促进细菌感染。然而，在豆科植物 - 根瘤菌共生的背景下，根瘤菌效应蛋白在调节植物共生途径中的作用在很大程度上仍未被探索。在这里，我们表明，NGR234的YopT型半胱氨酸蛋白酶NopT通过与两种结瘤因子受体（NFR1和NFR5）结合，直接靶向植物的共生信号通路。NopT抑制NFR1 / NFR5共表达在中引发的细胞死亡。全长NopT与NFR1和NFR5发生物理相互作用。NopT在体外和体内都能蛋白水解切割NFR5，但由于磷酸化可被NFR1灭活。NopT在介导根瘤菌感染中起重要作用。自切割的NopT保留切割NFR5的能力，但不再与NFR1相互作用。有趣的是，某些物种的基因组仅含有编码没有自切割位点的截短蛋白的基因。这些结果揭示了根瘤菌和豆科植物之间复杂的相互作用，其中根瘤菌效应蛋白酶靶向NFR5以抑制共生信号。NFR1似乎通过使效应蛋白磷酸化来抵消这一过程。这一发现突出了细菌效应蛋白在调节植物信号通路中的作用，并开辟了开发与激酶相互作用的蛋白酶以微调细胞信号过程的前景。
