Studying the Mechanism of Plasmopara viticola RxLR Effectors on Suppressing Plant Immunity

Jiang, Xiang; Li, Xinlong; Wu, Jiao; Yin, Ling; Zhang, Yali; Lu, Jiang

doi:10.3389/fmicb.2016.00709

Cited by 54 publications

(78 citation statements)

References 64 publications

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“…Suppression of Pattern Triggered Immunity (PTI) is a good marker to test the role of a given effector in virulence. It would be interesting to test whether P. halstedii RXLR or CRN effectors are able to suppress PTI induced by Phytophthora infestans infestin INF1, for example, as does the Phytophthora infestans Avr3A RXLR effector (Bos et al, 2006) and more recently, several RXLR from P. viticola (Xiang et al, 2016). …”

Section: Discussionmentioning

confidence: 99%

RXLR and CRN Effectors from the Sunflower Downy Mildew Pathogen Plasmopara halstedii Induce Hypersensitive-Like Responses in Resistant Sunflower Lines

et al. 2016

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Plasmopara halstedii is an obligate biotrophic oomycete causing downy mildew disease on sunflower, Helianthus annuus, an economically important oil crop. Severe symptoms of the disease (e.g., plant dwarfism, leaf bleaching, sporulation and production of infertile flower) strongly impair seed yield. Pl resistance genes conferring resistance to specific P. halstedii pathotypes were located on sunflower genetic map but yet not cloned. They are present in cultivated lines to protect them against downy mildew disease. Among the 16 different P. halstedii pathotypes recorded in France, pathotype 710 is frequently found, and therefore continuously controlled in sunflower by different Pl genes. High-throughput sequencing of cDNA from P. halstedii led us to identify potential effectors with the characteristic RXLR or CRN motifs described in other oomycetes. Expression of six P. halstedii putative effectors, five RXLR and one CRN, was analyzed by qRT-PCR in pathogen spores and in the pathogen infecting sunflower leaves and selected for functional analyses. We developed a new method for transient expression in sunflower plant leaves and showed for the first time subcellular localization of P. halstedii effectors fused to a fluorescent protein in sunflower leaf cells. Overexpression of the CRN and of 3 RXLR effectors induced hypersensitive-like cell death reactions in some sunflower near-isogenic lines resistant to pathotype 710 and not in susceptible corresponding lines, suggesting they could be involved in Pl loci-mediated resistances.

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Section: Discussionmentioning

confidence: 99%

RXLR and CRN Effectors from the Sunflower Downy Mildew Pathogen Plasmopara halstedii Induce Hypersensitive-Like Responses in Resistant Sunflower Lines

et al. 2016

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“…After being secreted by oomycetous pathogens, the RXLR effectors are transported to a range of subcellular localizations in plant cells, including the nucleus, cytoplasm, or plasma membrane, which often associates with their functions and/or mode of action (McLellan et al, 2013;Xiang et al, 2016). The study of subcellular localization of RXLR effectors from Phytophthora infestans revealed that the nucleocytoplasmic distribution in plant cells is the most common pattern (Wang et al, 2019a).…”

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confidence: 99%

An RXLR effector PlAvh142 from Peronophythora litchii triggers plant cell death and contributes to virulence

Situ

Jiang

Fan

et al. 2020

Molecular Plant Pathology

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Litchi downy blight, caused by the phytopathogenic oomycete Peronophythora litchii, results in tremendous economic loss in litchi production every year. To successfully colonize the host cell, Phytophthora species secret hundreds of RXLR effectors that interfere with plant immunity and facilitate the infection process. Previous work has already predicted 245 candidate RXLR effector‐encoding genes in P. litchii, 212 of which have been cloned and tested for plant cell death‐inducing activity in this study. We found three such RXLR effectors could trigger plant cell death through transient expression in Nicotiana benthamiana. Further experiments demonstrated that PlAvh142 could induce cell death and immune responses in several plants. We also found that PlAvh142 localized in both the cytoplasm and nucleus of plant cells. The cytoplasmic localization was critical for its cell death‐inducing activity. Moreover, deletion either of the two internal repeats in PlAvh142 abolished the cell death‐inducing activity. Virus‐induced gene silencing assays showed that cell death triggered by PlAvh142 was dependent on the plant transduction components RAR1 (require for Mla12 resistance), SGT1 (suppressor of the G2 allele of skp1) and HSP90 (heat shock protein 90). Finally, knockout of PlAvh142 resulted in significantly attenuated P. litchii virulence on litchi plants, whereas the PlAvh142‐overexpressed mutants were more aggressive. These data indicated that PlAvh142 could be recognized in plant cytoplasm and is an important virulence RXLR effector of P. litchii.

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“…B, see Supporting Information). The expression pattern of PvRXLR131 was similar to that of the second group of PvRXLRs (Xiang et al ., ), and these genes were highly expressed during the earlier infection stages. In addition, PvRXLR131 was successfully detected in 48 P. viticola isolates (Fig.…”

Section: Resultsmentioning

confidence: 98%

“…Functional genomic studies have been carried out to characterize RXLR effectors. Notably, suppression of host immunity seems to be a major function of most effectors, as was demonstrated in the model plant Nicotiana benthamiana by monitoring their ability to suppress elicitor‐triggered cell death or to enhance pathogen leaf colonisation and in the bacteria Pseudomonas syringae by assessing their ability to promote pathogen pathogenicity (Fabro et al ., ; Liu et al ., ; Wang et al ., , ; Xiang et al ., ). RXLR effectors target diverse pathways within the host cell to suppress plant immunity, such as preventing secretion of defence‐related proteases (Bozkurt et al ., ), reducing the accumulation of reactive oxygen species around invasion sites (Dong et al ., ), perturbing mitogen‐activated protein kinase (MAPK) pathways (King et al ., ), supporting or promoting the activity of negative immune regulators (Boevink et al ., ; Murphy et al ., ), suppressing RNA silencing and reducing accumulation of small RNAs (Qiao et al ., , ), and reprograming pre‐mRNA splicing (Huang et al ., ).…”

Section: Introductionmentioning

confidence: 97%

Plasmopara viticola effector PvRXLR131 suppresses plant immunity by targeting plant receptor‐like kinase inhibitor BKI1

Xia

Liu

Song

et al. 2019

Molecular Plant Pathology

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Summary The grapevine downy mildew pathogen Plasmopara viticola secretes a set of RXLR effectors (PvRXLRs) to overcome host immunity and facilitate infection, but how these effectors function is unclear. Here, the biological function of PvRXLR131 was investigated via heterologous expression. Constitutive expression of PvRXLR131 in Colletotrichum gloeosporioides significantly enhanced its pathogenicity on grapevine leaves. Constitutive expression of PvRXLR131 in Arabidopsis promoted Pseudomonas syringae DC3000 and P. syringae DC3000 (hrcC‐) growth as well as suppressed defence‐related callose deposition. Transient expression of PvRXLR131 in Nicotiana benthamiana leaves could also suppress different elicitor‐triggered cell death and inhibit plant resistance to Phytophthora capsici. Further analysis revealed that PvRXLR131 interacted with host Vitis vinifera BRI1 kinase inhibitor 1 (VvBKI1), and its homologues in N. benthamiana (NbBKI1) and Arabidopsis (AtBKI1). Moreover, bimolecular fluorescence complementation analysis revealed that PvRXLR131 interacted with VvBKI1 in the plasma membrane. Deletion assays showed that the C‐terminus of PvRXLR131 was responsible for the interaction and mutation assays showed that phosphorylation of a conserved tyrosine residue in BKI1s disrupted the interaction. BKI1 was a receptor inhibitor of growth‐ and defence‐related brassinosteroid (BR) and ERECTA (ER) signalling. When silencing of NbBKI1 in N. benthamiana, the virulence function of PvRXLR131 was eliminated, demonstrating that the effector activity is mediated by BKI1. Moreover, PvRXLR131‐transgenic plants displayed BKI1‐overexpression dwarf phenotypes and suppressed BR and ER signalling. These physiological and genetic data clearly demonstrate that BKI1 is a virulence target of PvRXLR131. We propose that P. viticola secretes PvRXLR131 to target BKI1 as a strategy for promoting infection.

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Studying the Mechanism of Plasmopara viticola RxLR Effectors on Suppressing Plant Immunity

Cited by 54 publications

References 64 publications

RXLR and CRN Effectors from the Sunflower Downy Mildew Pathogen Plasmopara halstedii Induce Hypersensitive-Like Responses in Resistant Sunflower Lines

RXLR and CRN Effectors from the Sunflower Downy Mildew Pathogen Plasmopara halstedii Induce Hypersensitive-Like Responses in Resistant Sunflower Lines

An RXLR effector PlAvh142 from Peronophythora litchii triggers plant cell death and contributes to virulence

Plasmopara viticola effector PvRXLR131 suppresses plant immunity by targeting plant receptor‐like kinase inhibitor BKI1

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