Deciphering the functions of three Phytophthora cactorum RXLR effectors involved in strawberry colonization
Authors
Anupam Gogoi (presenting author) [1]
Bikal Ghimire [2]
Mandeep Poudel [2]
Wyona Hager [1, 2]
André van Eerde [1]
May Bente Brurberg [1, 2]
Affiliations
- Department of Molecular Plant Biology, Norwegian Institute of Bioeconomy Research (NIBIO), Ås, Norway
Email (presenting author): anupam.gogoi@nibio.no - Department of Plant Sciences, Norwegian University of Life Sciences (NIBIO), Ås, Norway
Keywords
Oomycetes; dsRNA; plant immune suppression and defence; strawberry; N. benthamiana
Abstract
Phytophthora cactorum is a destructive pathogen of numerous fruit, ornamental, and landscape plants. Its genome encodes hundreds of RXLR effectors, which are secreted proteins and in general known to manipulate host cell processes and dampen immune responses. However, the functions of most P. cactorum RXLR effectors during plant colonization remain poorly understood. We characterized twenty RXLR effectors from P. cactorum expressed during infection of strawberry crown tissue. Seven effectors triggered cell death and enhanced callose deposition when transiently expressed in Nicotiana benthamiana, indicating activation of the plant immunity. Among the remaining 13 effectors, PcRXLR11 and PcRXLR14 supressed P. infestans INF1-induced cell death, whereas PcRXLR17 enhanced INF1-triggered cell death. Infection assays showed that PcRXLR11, which suppressed cell death, enhanced P. cactorum virulence. N-terminal YFP tagging of PcRXLR11, PcRXLR14 and PcRXLR17 revealed varied subcellular localisations including chloroplast, cytoplasm and/or plasma membrane. All three effector genes were upregulated during infection of strawberry leaves relative to the mycelial growth. Exogenous application of dsRNA designed to target effector transcripts reduced pathogen colonization in strawberry leaves, indicating that these effectors are required for successful infection. Overall, our results demonstrate that key P. cactorum RXLR effectors manipulate host immunity and contribute to pathogen virulence.
Funding
The author(s) declare that financial support was received for the research, authorship, and/or publication of this research work. The work was also supported by NIBIO (basic funding) and the Research Council of Norway, grant number 326212. BG was funded by the European Union’s Horizon 2020 (H2020) Marie Skłodowska-Curie Actions Innovative Training Networks PROTECTA H2020-MSCA-ITN-2017 call, under the grant agreement number 766048.