A Phytophthora infestans RXLR effector targets plant PP1c isoforms that promote late blight disease

Petra C. Boevink, Xiaodan Wang, Hazel McLellan, Qin He, Shaista Naqvi, Miles R. Armstrong, Wei Zhang, Ingo Hein, Eleanor M. Gilroy, Zhendong Tian and Paul R. J. Birch ()
Additional contact information
Petra C. Boevink: James Hutton Institute
Xiaodan Wang: James Hutton Institute
Hazel McLellan: College of Life Science, University of Dundee (at JHI)
Qin He: College of Life Science, University of Dundee (at JHI)
Shaista Naqvi: James Hutton Institute
Miles R. Armstrong: James Hutton Institute
Wei Zhang: Key Laboratory of Horticultural Plant Biology (at HAU), Ministry of Education, National Center for Vegetable Improvement (Central China), Huazhong Agricultural University
Ingo Hein: James Hutton Institute
Eleanor M. Gilroy: James Hutton Institute
Zhendong Tian: Key Laboratory of Horticultural Plant Biology (at HAU), Ministry of Education, National Center for Vegetable Improvement (Central China), Huazhong Agricultural University
Paul R. J. Birch: James Hutton Institute

Nature Communications, 2016, vol. 7, issue 1, 1-14

Abstract: Abstract Plant pathogens deliver effectors to alter host processes. Knowledge of how effectors target and manipulate host proteins is critical to understand crop disease. Here, we show that in planta expression of the RXLR effector Pi04314 enhances leaf colonization by Phytophthora infestans via activity in the host nucleus and attenuates induction of jasmonic and salicylic acid-responsive genes. Pi04314 interacts with three host protein phosphatase 1 catalytic (PP1c) isoforms, causing their re-localization from the nucleolus to the nucleoplasm. Re-localization of PP1c-1 also occurs during infection and is dependent on an R/KVxF motif in the effector. Silencing the PP1c isoforms or overexpression of a phosphatase-dead PP1c-1 mutant attenuates infection, demonstrating that host PP1c activity is required for disease. Moreover, expression of PP1c–1mut abolishes enhanced leaf colonization mediated by in planta Pi04314 expression. We argue that PP1c isoforms are susceptibility factors forming holoenzymes with Pi04314 to promote late blight disease.

Date: 2016
References: Add references at CitEc
Citations: View citations in EconPapers (1)

Downloads: (external link)
https://www.nature.com/articles/ncomms10311 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms10311

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms10311

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().