Journal
MOLECULAR PLANT
Volume 8, Issue 9, Pages 1385-1395Publisher
CELL PRESS
DOI: 10.1016/j.molp.2015.04.012
Keywords
effector-triggered susceptibility; oomycete; plant disease; late blight
Categories
Funding
- Biotechnology and Biological Sciences Research Council (BBSRC) [BB/G015244/1, BB/K018183/1, BB/L026880/1]
- Scottish Government Rural and Environment Science and Analytical Services Division (RESAS)
- China Scholarship Council (CSC)
- BBSRC [BB/L026880/1, BB/G015244/1, BB/K018183/1] Funding Source: UKRI
- Biotechnology and Biological Sciences Research Council [BB/L026880/1, BB/K018183/1, BB/G015244/1] Funding Source: researchfish
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Plant pathogens deliver effector proteins that alter host processes to create an environment conducive to colonization. Attention has focused on identifying the targets of effectors and how their manipulation facilitates disease. RXLR effector Pi04089 from the potato blight pathogen Phytophthora infestans accumulates in the host nucleus and enhances colonization when transiently expressed in planta. Its nuclear localization is required for enhanced P. infestans colonization. Pi04089 interacts in yeast and in planta with a putative potato K-homology (KH) RNA-binding protein, StKRBP1. Co-localization of Pi04089 and StKRBP1, and bimolecular fluorescence complementation between them, indicate they associate at nuclear speckles. StKRBP1 protein levels increased when it was co-expressed with Pi04089. Indeed, such accumulation of StKRBP1 was observed also on the first day of leaf colonization by the pathogen. Remarkably, overexpression of StKRBP1 significantly enhances P. infestans infection. Mutation of the nucleotide-binding motif GxxG to GDDG in all three KH domains of StKRBP1 abolishes its interaction with Pi04089, its localization to nuclear speckles, and its increased accumulation when co-expressed with the effector. Moreover, the mutant StKRBP1 protein no longer enhances leaf colonization by P. infestans, implying that nucleotide binding is likely required for this activity. We thus argue that StKRBP1 can be regarded as a susceptibility factor, as its activity is beneficial to the pathogen.
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