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Genome sequences of several economically important phytopathogenic oomycetes have revealed the presence of large families of so-called RXLR effectors. Functional screens have identified RXLR effector repertoires that either compromise or induce plant defense responses. However, limited information is available about the molecular mechanisms underlying the modes of action of these effectors in planta. The perception of highly conserved pathogen- or microbe-associated molecular patterns (PAMPs/MAMPs), such as flg22, triggers converging signaling pathways recruiting MAP kinase cascades and inducing transcriptional re-programming, yielding a generic anti-microbial response. We used a highly synchronizable, pathogen-free protoplast-based assay to identify a set of RXLR effectors from Phytophthora infestans (PiRXLRs), the causal agent of potato and tomato light blight that manipulate early stages of flg22-triggered signaling. Of thirty-three tested PiRXLR effector candidates, eight, called Suppressor of early Flg22-induced Immune response (SFI), significantly suppressed flg22-dependent activation of a reporter gene under control of a typical MAMP-inducible promoter (pFRK1-Luc) in tomato protoplasts. We extended our analysis to Arabidopsis thaliana, a non-host plant species of P. infestans. From the aforementioned eight SFI effectors, three appeared to share similar functions in both Arabidopsis and tomato by suppressing transcriptional activation of flg22-induced marker genes downstream of post-translational MAP kinase activation. A further three effectors interfere with MAMP signaling at, or upstream of, the MAP kinase cascade in tomato, but not in Arabidopsis. Transient expression of the SFI effectors in Nicotiana benthamiana enhances susceptibility to P. infestans and, for the most potent effector, SFI1, nuclear localization is required for both suppression of MAMP signaling and virulence function. The present study provides a framework to decipher the molecular mechanisms underlying the manipulation of host MAMP-triggered immunity (MTI) by P. infestans and to understand the basis of host versus non-host resistance in plants towards P. infestans.
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http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3999189 | PMC |
http://dx.doi.org/10.1371/journal.ppat.1004057 | DOI Listing |
Plant Pathol J
December 2024
Department of Applied Biology, Chungnam National University, Daejeon 34134, Korea.
Plasmopara viticola causes grape downy mildew, one of the most notorious diseases of cultivated grapes that damage vineyards worldwide. The pathogen secretes various effector molecules to infect and modulate the host biological processes. In this study, we aimed to evaluate the roles of KPvRxLR27, an arginine-any amino acid-leucine-arginine (RxLR) effector isolated from P.
View Article and Find Full Text PDFMycobiology
November 2024
Department of Applied Biology, Chungnam National University, Daejeon, South Korea.
is a significant phytopathogen causing downy mildew disease in cucurbit crops. Understanding the molecular mechanisms underlying the interaction between and its host is essential for developing effective disease management strategies. RxLR effectors, secreted by pathogens, play a crucial role in modulating host immunity.
View Article and Find Full Text PDFJ Fungi (Basel)
October 2024
Biology and Breeding Research Program, Colombian Oil Palm Research Center, Cenipalma, Calle 98 No. 70-91, Piso 14, Bogotá 111121, Colombia.
is the pathogen causing bud rot in oil palm ). This pathogen secretes effector proteins that manipulate host defenses, contributing to disease progression. In this study, we systematically investigated the role of specific effector proteins in suppressing programmed cell death (PCD) in oil palm leaflets.
View Article and Find Full Text PDFNew Phytol
November 2024
School of Biological Science, University of Canterbury, Private Bag 4800, Christchurch, 8140, New Zealand.
Mol Cells
December 2024
Department of Agriculture, Forestry and Bioresources, Plant Genomics and Breeding Institute, College of Agriculture and Life Science, Seoul National University, Seoul 08826, Republic of Korea; Plant Immunity Research Center, College of Agriculture and Life Science, Seoul National University, Seoul 08826, Republic of Korea. Electronic address:
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