The RXLR effector PpE18 of Phytophthora parasitica is a virulence factor and suppresses peroxisome membrane-associated ascorbate peroxidase NbAPX3-1-mediated plant immunity

© 2024 The Authors. New Phytologist © 2024 New Phytologist Foundation.

Bibliographische Detailangaben
Veröffentlicht in:The New phytologist. - 1979. - 243(2024), 4 vom: 14. Juli, Seite 1472-1489
1. Verfasser: Cao, Yimeng (VerfasserIn)
Weitere Verfasser: Zhang, Qiang, Liu, Yuan, Yan, Tiantian, Ding, Liwen, Yang, Yang, Meng, Yuling, Shan, Weixing
Format: Online-Aufsatz
Sprache:English
Veröffentlicht: 2024
Zugriff auf das übergeordnete Werk:The New phytologist
Schlagworte:Journal Article Phytophthora parasitica NbAPX3‐1 PpE18 ROS‐scavenging activity RXLR effector peroxisome plant immunity Reactive Oxygen Species Ascorbate Peroxidases mehr... EC 1.11.1.11 Virulence Factors
Beschreibung
Zusammenfassung:© 2024 The Authors. New Phytologist © 2024 New Phytologist Foundation.
Phytophthora parasitica causes diseases on a broad range of host plants. It secretes numerous effectors to suppress plant immunity. However, only a few virulence effectors in P. parasitica have been characterized. Here, we highlight that PpE18, a conserved RXLR effector in P. parasitica, was a virulence factor and suppresses Nicotiana benthamiana immunity. Utilizing luciferase complementation, co-immunoprecipitation, and GST pull-down assays, we determined that PpE18 targeted NbAPX3-1, a peroxisome membrane-associated ascorbate peroxidase with reactive oxygen species (ROS)-scavenging activity and positively regulates plant immunity in N. benthamiana. We show that the ROS-scavenging activity of NbAPX3-1 was critical for its immune function and was hindered by the binding of PpE18. The interaction between PpE18 and NbAPX3-1 resulted in an elevation of ROS levels in the peroxisome. Moreover, we discovered that the ankyrin repeat-containing protein NbANKr2 acted as a positive immune regulator, interacting with both NbAPX3-1 and PpE18. NbANKr2 was required for NbAPX3-1-mediated disease resistance. PpE18 competitively interfered with the interaction between NbAPX3-1 and NbANKr2, thereby weakening plant resistance. Our results reveal an effective counter-defense mechanism by which P. parasitica employed effector PpE18 to suppress host cellular defense, by suppressing biochemical activity and disturbing immune function of NbAPX3-1 during infection
Beschreibung:Date Completed 18.07.2024
Date Revised 19.07.2024
published: Print-Electronic
Citation Status MEDLINE
ISSN:1469-8137
DOI:10.1111/nph.19902