A <i>Phytophthora capsici</i> effector suppresses plant immunity via interaction with EDS1

Li, Qi; Wang, Ji; Bai, Tian; Zhang, Ming; Jia, Yuling; Shen, Danyu; Zhang, Meixiang; Dou, Daolong

doi:10.1111/mpp.12912

Cited by 45 publications

(25 citation statements)

References 48 publications

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“…These differential expressions are probably P. capsici -specific because their expression was not affected by inoculation with Phytophthora infestans , pepper mottle virus, or tobacco mosaic virus [ 46 ]. Reverse genetic studies stress the function of many other factors in P. capsici resistance, e.g., CaRGA2 [ 47 ], EDS1 [ 11 ], CaChiIV1 [ 48 ], CaAP2/ERF064 [ 49 ], and squamosal promoter binding protein (SBP) [ 50 ]. However, no significant response of these genes was identified at the locus Pc5.1 .…”

Section: Discussionmentioning

confidence: 99%

“…P. capsici has even become a model pathogen in the study of plant-microbe interactions due to its wide range of hosts, including potato, tomato, cucurbits, beans, Arabidopsis and tobacco [ 6 8 ]. On the attack side, Phytophthora pathogens secrete and dispatch effectors such as RxLR into host cells, which paralyse the plant host immune system, including basal immune system named pattern-triggered immunity (PTI) [ 9 ], endoplasmic reticulum (ER) stress-mediated plant immunity [ 10 ], and the EDS-PAD4 immune signaling pathway [ 11 ]. In addition, pathogenic effectors can also disturb histone acetylation [ 12 ] and ethylene biosynthesis [ 13 ].…”

Section: Introductionmentioning

confidence: 99%

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The dissection of R genes and locus Pc5.1 in Phytophthora capsici infection provides a novel view of disease resistance in peppers

Liao

Hao

et al. 2021

BMC Genomics

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Background Phytophthora capsici root rot (PRR) is a disastrous disease in peppers (Capsicum spp.) caused by soilborne oomycete with typical symptoms of necrosis and constriction at the basal stem and consequent plant wilting. Most studies on the QTL mapping of P. capsici resistance suggested a consensus broad-spectrum QTL on chromosome 5 named Pc.5.1 regardless of P. capsici isolates and resistant resources. In addition, all these reports proposed NBS-ARC domain genes as candidate genes controlling resistance. Results We screened out 10 PRR-resistant resources from 160 Capsicum germplasm and inspected the response of locus Pc.5.1 and NBS-ARC genes during P. capsici infection by comparing the root transcriptomes of resistant pepper 305R and susceptible pepper 372S. To dissect the structure of Pc.5.1, we anchored genetic markers onto pepper genomic sequence and made an extended Pc5.1 (Ext-Pc5.1) located at 8.35 Mb–38.13 Mb on chromosome 5 which covered all Pc5.1 reported in publications. A total of 571 NBS-ARC genes were mined from the genome of pepper CM334 and 34 genes were significantly affected by P. capsici infection in either 305R or 372S. Only 5 inducible NBS-ARC genes had LRR domains and none of them was positioned at Ext-Pc5.1. Ext-Pc5.1 did show strong response to P. capsici infection and there were a total of 44 differentially expressed genes (DEGs), but no candidate genes proposed by previous publications was included. Snakin-1 (SN1), a well-known antimicrobial peptide gene located at Pc5.1, was significantly decreased in 372S but not in 305R. Moreover, there was an impressive upregulation of sugar pathway genes in 305R, which was confirmed by metabolite analysis of roots. The biological processes of histone methylation, histone phosphorylation, DNA methylation, and nucleosome assembly were strongly activated in 305R but not in 372S, indicating an epigenetic-related defense mechanism. Conclusions Those NBS-ARC genes that were suggested to contribute to Pc5.1 in previous publications did not show any significant response in P. capsici infection and there were no significant differences of these genes in transcription levels between 305R and 372S. Other pathogen defense-related genes like SN1 might account for Pc5.1. Our study also proposed the important role of sugar and epigenetic regulation in the defense against P. capsici.

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Section: Discussionmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

The dissection of R genes and locus Pc5.1 in Phytophthora capsici infection provides a novel view of disease resistance in peppers

Liao

Hao

et al. 2021

BMC Genomics

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“…Further research revealed EDS1 as a positive regulator of plant immunity that interacts with Phytoalexin Deficient 4 (PAD4) and this EDS1-PAD4 complex plays a key role in SA accumulation and also regulate SA mediated defense (Wiermer et al, 2005). PcAvh103 is reported to promote P. capsici infection by binding with EDS1 and disrupting EDS1-PAD4 (Li et al, 2020). EDS1-PAD4 operates upstream of the SA pathway, whereas NPR1 (nonexpressor of pathogenesis related1) is a SA receptor that operates downstream signaling.…”

Section: Modulation Of Defense Hormones Signalingmentioning

confidence: 99%

The PTI to ETI Continuum in Phytophthora-Plant Interactions

et al. 2020

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Phytophthora species are notorious pathogens of several economically important crop plants. Several general elicitors, commonly referred to as Pathogen-Associated Molecular Patterns (PAMPs), from Phytophthora spp. have been identified that are recognized by the plant receptors to trigger induced defense responses in a process termed PAMP-triggered Immunity (PTI). Adapted Phytophthora pathogens have evolved multiple strategies to evade PTI. They can either modify or suppress their elicitors to avoid recognition by host and modulate host defense responses by deploying hundreds of effectors, which suppress host defense and physiological processes by modulating components involved in calcium and MAPK signaling, alternative splicing, RNA interference, vesicle trafficking, cell-to-cell trafficking, proteolysis and phytohormone signaling pathways. In incompatible interactions, resistant host plants perceive effector-induced modulations through resistance proteins and activate downstream components of defense responses in a quicker and more robust manner called effector-triggered-immunity (ETI). When pathogens overcome PTI—usually through effectors in the absence of R proteins—effectors-triggered susceptibility (ETS) ensues. Qualitatively, many of the downstream defense responses overlap between PTI and ETI. In general, these multiple phases of Phytophthora-plant interactions follow the PTI-ETS-ETI paradigm, initially proposed in the zigzag model of plant immunity. However, based on several examples, in Phytophthora-plant interactions, boundaries between these phases are not distinct but are rather blended pointing to a PTI-ETI continuum.

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“…capsici effector PcAvh103 has been shown to interact with defense regulator enhanced disease susceptibility 1 (EDS1). The binding of PcAvh103 to the EDS1 lipase domain stops EDS1–PAD4 association, thus effectively preventing downstream signaling mediated by this complex ( Li et al., 2020 ). The RxLR effector PexRD54 from P .…”

Section: Effector Modes Of Actionmentioning

confidence: 99%

All Roads Lead to Susceptibility: The Many Modes of Action of Fungal and Oomycete Intracellular Effectors

McLellan

Boevink

et al. 2020

Plant Communications

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The ability to secrete effector proteins that can enter plant cells and manipulate host processes is a key determinant of what makes a successful plant pathogen. Here, we review intracellular effectors from filamentous (fungal and oomycete) phytopathogens and the host proteins and processes that are targeted to promote disease. We cover contrasting virulence strategies and effector modes of action. Filamentous pathogen effectors alter the fates of host proteins that they target, changing their stability, their activity, their location, and the protein partners with which they interact. Some effectors inhibit target activity, whereas others enhance or utilize it, and some target multiple host proteins. We discuss the emerging topic of effectors that target negative regulators of immunity or other plant proteins with activities that support susceptibility. We also highlight the commonly targeted host proteins that are manipulated by effectors from multiple pathogens, including those representing different kingdoms of life.

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A Phytophthora capsici effector suppresses plant immunity via interaction with EDS1

Cited by 45 publications

References 48 publications

The dissection of R genes and locus Pc5.1 in Phytophthora capsici infection provides a novel view of disease resistance in peppers

The dissection of R genes and locus Pc5.1 in Phytophthora capsici infection provides a novel view of disease resistance in peppers

The PTI to ETI Continuum in Phytophthora-Plant Interactions

All Roads Lead to Susceptibility: The Many Modes of Action of Fungal and Oomycete Intracellular Effectors

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