Abstract
Grapevine downy mildew, caused by oomycete fungus Plasmopara viticola, is one of the most devastating diseases of grapes across the major production regions of the world. Although many putative effector molecules have been identified from this pathogen, the functions of the majority of these are still unknown. In this study, we analyzed the potential function of 26 P. viticola effectors from the highly virulent strain YL. Using transient expression in leaf cells of the tobacco Nicotiana benthamiana, we found that the majority of the effectors could suppress cell death triggered by BAX and INF1, while seven could induce cell death. The subcellular localization of effectors in N. benthamiana was consistent with their localization in cells of Vitis vinifera. Those effectors that localized to the nucleus (17/26) showed a variety of subnuclear localization. Ten of the effectors localized predominantly to the nucleolus, whereas the remaining seven localized to nucleoplasm. Interestingly, five of the effectors were strongly related in sequence and showed identical subcellular localization, but had different functions in N. benthamiana leaves and expression patterns in grapevine in response to P. viticola. This study highlights the potential functional diversity of P. viticola effectors.
Highlights
Grapevine downy mildew, caused by the oomycete Plasmopara viticola
We studied the virulence function of 26 of the RxLR effectors by transient expression in N. benthamiana cells. We examined both their ability to suppress cell death induced by INF1 and BAX, and their subcellular localization, both in N. benthamiana and V. vinifera
The sequence of the putative P. viticola RxLR effectors in this paper can be found in GenBank date library of National Center for Biotechnology Information (NCBI), and all accession numbers were listed in Supplementary Table S2
Summary
Grapevine downy mildew, caused by the oomycete Plasmopara viticola Pathogenic oomycetes secrete effector molecules into the plant to disturb plant innate immunity, facilitating penetration and colonization (Judelson and Blanco, 2005; Kamoun, 2006; Tyler et al, 2006; Birch et al, 2009; Bozkurt et al, 2012; King et al, 2014). These effectors are divided into two important classes, apoplastic and cytoplasmic effectors. An exact RxLR-EER sequence is not always required for translocation to the host cell (Dou et al, 2008; Tian et al, 2011; Chen et al, 2013; Ye et al, 2015)
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