Chen Tao, Duan Liujian, Zhou Bo, Yu Haixiang, Zhu Hui, Cao Yangrong, Zhang Zhongming
State Key Laboratory of Agricultural Microbiology, Huazhong Agricultural UniversityWuhan, China.
The Provincial Key Laboratory of Plant Pathology of Hubei Province, College of Plant Science and Technology, Huazhong Agricultural UniversityWuhan, China.
Front Microbiol. 2017 May 30;8:973. doi: 10.3389/fmicb.2017.00973. eCollection 2017.
Suppression of host innate immunity appears to be required for the establishment of symbiosis between rhizobia and host plants. In this study, we established a system that included a host plant, a bacterial pathogen and a symbiotic rhizobium to study the role of innate immunity during symbiotic interactions. A pathogenic bacterium, pv. strain DC3000 ( DC3000), was shown to cause chlorosis in A17. strain Sm2011 (Sm2011) and DC3000 strain alone induced similar defense responses in However, when co-inoculated, Sm2011 specifically suppressed the defense responses induced by DC3000, such as MAPK activation and ROS production. Inoculation with Sm2011 suppressed the transcription of defense-related genes triggered by DC3000 infection, including the receptor of bacterial flagellin (), pathogenesis-related protein 10 (), and the transcription factor . Interestingly, inoculation with DC3000 specifically inhibited the expression of the symbiosis marker genes and and reduced the numbers of infection threads and nodules on A17 roots, indicating that DC3000 inhibits the establishment of symbiosis in In addition, defense-related genes, such as , , exhibited a transient increase in their expression in the early stage of symbiosis with Sm2011, but the expression dropped down to normal levels at later symbiotic stages. Our results suggest that plant innate immunity plays an antagonistic role in symbiosis by directly reducing the numbers of infection threads and nodules.
根瘤菌与宿主植物建立共生关系似乎需要抑制宿主的先天免疫。在本研究中,我们建立了一个包含宿主植物、细菌病原体和共生根瘤菌的系统,以研究先天免疫在共生相互作用中的作用。一种病原菌,丁香假单胞菌番茄致病变种菌株DC3000(DC3000),被证明会在A17中引起黄化。单独接种大豆根瘤菌Sm2011菌株(Sm2011)和DC3000菌株在A17中诱导了相似的防御反应。然而,当共同接种时,Sm2011特异性地抑制了DC3000诱导的防御反应,如丝裂原活化蛋白激酶(MAPK)激活和活性氧(ROS)产生。接种Sm2011抑制了DC3000感染引发的防御相关基因的转录,包括细菌鞭毛蛋白受体(FLS2)、病程相关蛋白10(PR10)和转录因子(WRKY33)。有趣的是,接种DC3000特异性地抑制了共生标记基因(NIN)和(ERF)的表达,并减少了A17根上感染线和根瘤的数量,这表明DC3000抑制了A17中的共生建立。此外,防御相关基因,如(FLS2)、(PR10),在与Sm2011共生的早期阶段其表达短暂增加,但在共生后期下降到正常水平。我们的结果表明,植物先天免疫通过直接减少感染线和根瘤的数量在共生中起拮抗作用。