A Ralstonia solanacearum effector targets TGA transcription factors to subvert salicylic acid signaling. Issue 5 (19th January 2022)

• Record Type: Journal Article
• Authors: Qi, Peipei; Huang, Mengling; Hu, Xuehan; Zhang, Ying; Wang, Ying; Li, Pengyue; Chen, Shiyun; Zhang, Dan; Cao, Sen; Zhu, Wanting; Xie, Jiatao; Cheng, Jiasen; Fu, Yanping; Jiang, Daohong; Yu, Xiao; Li, Bo
• Is Part Of: The Plant Cell. Volume 34:Issue 5(2022)
• Page Start: 1666
• Page End: 1683
• Publication Date: 2022-01-19
• DOI: 10.1093/plcell/koac015
• Languages: English
• ISSNs: 1040-4651

Abstract

Abstract: The bacterial pathogen Ralstonia solanacearum causes wilt disease on Arabidopsis thaliana and tomato ( Solanum lycopersicum ). This pathogen uses type III effectors to inhibit the plant immune system; however, how individual effectors interfere with plant immune responses, including transcriptional reprograming, remain elusive. Here, we show that the type III effector RipAB targets Arabidopsis TGACG SEQUENCE-SPECIFIC BINDING PROTEIN (TGA) transcription factors, the central regulators of plant immune gene regulation, via physical interaction in the nucleus to dampen immune responses. RipAB was required for R. solanacearum virulence on wild-type tomato and Arabidopsis but not Arabidopsis tga1 tga4 and tga2 tga5 tga6 mutants. Stable expression of RipAB in Arabidopsis suppressed the pathogen-associated molecular pattern-triggered reactive oxygen species (ROS) burst and immune gene induction as well as salicylic acid (SA) regulons including RBOHD and RBOHF, responsible for ROS production, all of which were phenocopied by the tga1 tga4 and tga2 tga5 tga6 mutants. We found that TGAs directly activate RBOHD and RBOHF expression and that RipAB inhibits this through interfering with the recruitment of RNA polymerase II. These results suggest that TGAs are the bona fide and major virulence targets of RipAB, which disrupts SA signaling by inhibiting TGA activity to achieve successful infection. Abstract : Ralstonia solanacearum type III effector RipAB directly interacts with TGAs to interfere with the recruitment of RNA Pol II at TGA-regulons, thereby disrupting immune gene expression in Arabidopsis.