Evolutionarily distinct resistance proteins detect a pathogen effector through its association with different host targets

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Wang, Haixia, Trusch, Franziska, Turnbull, Dionne, Aguilera-Galvez, Carolina, Breen, Susan, Naqvi, Shaista, Jones, Jonathan D. G., Hein, Ingo, Tian, Zhendong, Vleeshouwers, Vivianne, Gilroy, Eleanor and Birch, Paul R. J. (2021) Evolutionarily distinct resistance proteins detect a pathogen effector through its association with different host targets. New Phytologist, 232 (3). pp. 1368-1381. ISSN 0028-646X

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Abstract

Knowledge of the evolutionary processes which govern pathogen recognition is critical to understanding durable disease resistance. We determined how Phytophthora infestans effector PiAVR2 is recognised by evolutionarily distinct resistance proteins R2 and Rpi-mcq1. We employed yeast two-hybrid, co-immunoprecipitation, virus-induced gene silencing, transient overexpression, and phosphatase activity assays to investigate the contributions of BSL phosphatases to R2- and Rpi-mcq1-mediated hypersensitive response (R2 HR and Rpi-mcq1 HR, respectively). Silencing PiAVR2 target BSL1 compromises R2 HR. Rpi-mcq1 HR is compromised only when BSL2 and BSL3 are silenced. BSL1 overexpression increases R2 HR and compromises Rpi-mcq1. However, overexpression of BSL2 or BSL3 enhances Rpi-mcq1 and compromises R2 HR. Okadaic acid, which inhibits BSL phosphatase activity, suppresses both recognition events. Moreover, expression of a BSL1 phosphatase-dead (PD) mutant suppresses R2 HR, whereas BSL2-PD and BSL3-PD mutants suppress Rpi-mcq1 HR. R2 interacts with BSL1 in the presence of PiAVR2, but not with BSL2 and BSL3, whereas no interactions were detected between Rpi-mcq1 and BSLs. Thus, BSL1 activity and association with R2 determine recognition of PiAVR2 by R2, whereas BSL2 and BSL3 mediate Rpi-mcq1 perception of PiAVR2. R2 and Rpi-mcq1 utilise distinct mechanisms to detect PiAVR2 based on association with different BSLs, highlighting central roles of these effector targets for both disease and disease resistance.

Item Type: Article
Additional Information: Funding Information: We are thankful for financial support from the Biotechnology and Biological Sciences Research Council (BBSRC) grants BB/P020569/1, BB/N009967/1 and BB/L026880/1, ERC‐Advanced grant PathEVome (787764), the Scottish Government Rural and Environment Science and Analytical Services Division (RESAS) and the National Natural Science Foundation of China (31761143007).
Uncontrolled Keywords: avirulence,cell death,effector-triggered immunity,nlr,plant immunity,plant pathogen co-evolution,potato late blight,resistance protein,physiology,plant science ,/dk/atira/pure/subjectarea/asjc/1300/1314
Faculty \ School: Faculty of Science > School of Biological Sciences
Faculty of Science > The Sainsbury Laboratory
UEA Research Groups: Faculty of Science > Research Groups > Plant Sciences
Related URLs:
Depositing User: LivePure Connector
Date Deposited: 22 Oct 2024 13:30
Last Modified: 01 Nov 2024 12:30
URI: https://ueaeprints.uea.ac.uk/id/eprint/97110
DOI: 10.1111/nph.17660

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