Phytophthora infestans effector PiAvr2 targets StBSLs to activate The Brassinosteroid pathway
E. GILROY (1), D. Turnbull (2), S. Naqvi (3), S. Breen (4), H. Wang (5), M. Malec (6), H. Mclellan (7), L. Welsh (8), P. Hedley (8), J. Stephens (8), F. Brunner (9), L. Yang (10), Z. Tian (5), J. Zhan (12), P. Birch (7) (1) The James Hutton Institute, Dundee, Scotland, United Kingdom; (10) Fujian Key Laboratory of Plant Virology, Fujian Agricultural and Forestry University, Fuzhou, China., China; (11) College of Horticulture and Forestry, Huazhong Agricultural University, Wuhan, China, China; (12) Fujian Key Laboratory of Plant Virology, Fujian Agricultural and Forestry University, Fuzhou, China., China; (2) The University of Dundee, Dundee, Scotland, United Kingdom; (3) James Hutton Ltd, United Kingdom; (4) The Australian National University, Australia; (5) College of Horticulture and Forestry, Huazhong Agricultural University, Wuhan, China, China; (6) Centre for Plant Molecular Biology, University of Tuebingen,, Germany; (7) The University of Dundee, United Kingdom; (8) The James Hutton Institute, United Kingdom; (9) Centre for Plant Molecular Biology, University of Tuebingen, Tuebingen, Germany, Germany
An emerging area in plant research focuses on antagonism between regulatory systems governing growth or immunity. Such crosstalk represents a point of vulnerability for pathogens to exploit. PiAVR2, an effector protein secreted by the notorious potato blight pathogen Phytophthora infestans, interacts with potato BSL1 implicated in growth-promoting brassinosteroid hormone signalling. Transient expression of StBSL1 in plants suppresses immunity and enhances P. infestans leaf colonisation, indicating that StBSL1 can be regarded as a susceptibility factor, activity of which promotes disease. We can now demonstrate that StBSL1 has phosphatase activity and that PiAVR2 does not appear to suppress that activity. We will present evidence that PiAVR2 also interacts with other StBSL family members which also have measurable phosphatase activity. StBSL family members show differential characteristics in terms of INF1 CD suppression and activity in the R2 HR. Interestingly, PiAVR2 can still suppress the INF1 CD in a BSL1 VIGS background but not when other StBSLs are silenced. We will report on progress examining the interactions between these StBSLs and PiAVR2. Plants expressing PiAVR2 exhibit transcriptional and phenotypic hallmarks of over-active brassinosteroid signalling, and have compromised immunity. The activity of PiAVR2 leads to up-regulation of a functional orthologue of HBI1, known to facilitate antagonism between brassinosteroid and immune responses. Transient expression of StHBI1-like compromises immunity and enhances leaf colonisation by P. infestans. We will highlight our current understanding of how PiAVR2 functions in promoting a growth and development pathway in order to antagonise plant immunity.
Abstract Number:
P16-450
Session Type:
Poster
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