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Activation and Suppression of Plant Immunity

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Front. Plant Sci. | doi: 10.3389/fpls.2018.00688

Differential suppression of Nicotiana benthamiana innate immune responses by transiently expressed Pseudomonas syringae type III effectors

  • 1Plant Molecular Genetics Department, Centro Nacional de Biotecnología (CNB), Spain
  • 2The Sainsbury Laboratory, United Kingdom
  • 3Institute of Genetics, Ludwig-Maximilians-Universität München, Germany
  • 4Department of Environmental Science, Botanical Institute, Universität Basel, Switzerland
  • 5Department of Botany and Plant Pathology, Oregon State University, United States
  • 6Center for Genome Research and Biocomputing, Oregon State University, United States
  • 7Plant Science Department, Plant Genomics and Breeding Institute and Research Institute of Agriculture and Life Sciences, College of Agriculture and Life Sciences, Seoul National University, South Korea
  • 8Research School of Biology, Australian National University, Australia

The plant pathogen Pseudomonas syringae injects about thirty different virulence proteins, so-called effectors, via a type III secretion system into plant cells to promote disease. Although some of these effectors are known to suppress either pattern-triggered immunity (PTI) or effector-triggered immunity (ETI), the mode of action of most of them remains unknown. Here, we used transient expression in Nicotiana benthamiana, to test the abilities of type III effectors of Pseudomonas syringae pv tomato (Pto) DC3000 and Pseudomonas syringae pv tabaci (Pta) 11528 to interfere with plant immunity. We monitored the sequential and rapid bursts of cytoplasmic Ca2+ and reactive oxygen species (ROS), the subsequent induction of defense gene expression, and promotion of cell death. We found that several effector proteins caused cell death, but independently of the known plant immune regulator NbSGT1, a gene essential for ETI. Furthermore, many effectors delayed or blocked the cell death-promoting activity of other effectors, thereby potentially contributing to pathogenesis. Secondly, a large number of effectors were able to suppress PAMP-induced defense responses. In the majority of cases, this resulted in suppression of all studied PAMP responses, suggesting that these effectors target common elements of PTI. However, effectors also targeted different steps within defense pathways and could be divided into three major groups based on their suppressive activities. Finally, the abilities of effectors of both Pto DC3000 and Pta 11528 to suppress plant immunity was conserved in most but not all cases. Overall, our data present a comprehensive picture of the mode of action of these effectors and indicate that most of them suppress plant defenses in various ways.

Keywords: Pseudomonas syringae, Type III effectors, PAMPS, PTI, Ca2+ burst, ROS, Defence gene expression, Cell Death, Nicotiana benthamiana., Pto DC3000, Pta 11528

Received: 25 Jan 2018; Accepted: 04 May 2018.

Edited by:

Zhengqing Fu, University of South Carolina, Columbia, United States

Reviewed by:

Frederik Börnke, Leibniz-Institut für Gemüse- und Zierpflanzenbau (IGZ), Germany
Brian H. Kvitko, University of Georgia, United States  

Copyright: © 2018 Gimenez-Ibanez, Hann, Chang, Segonzac, Boller and Rathjen. This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

* Correspondence: PhD. Selena Gimenez-Ibanez, Centro Nacional de Biotecnología (CNB), Plant Molecular Genetics Department, Darwin 3, Madrid, 28049, Spain, selena.gimenez@cnb.csic.es