The oomycete microbe-associated molecular pattern Pep-13 triggers SERK3/BAK1-independent plant immunity

Wang, Haixia; He, Huan; Qi, Yetong; McLellan, Hazel; Tian, Zhendong; Birch, Paul R. J.; Tian, Zhendong

doi:10.1007/s00299-018-2359-5

Cited by 13 publications

(10 citation statements)

References 45 publications

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“…Also, Arabidopsis bak1 mutants displayed reduced growth inhibition in response to flg22 17 . On the other hand, in accordance with our data, potato plants silenced for BAK1 with a StSERK3A -specific RNAi construct showed Pep-13-inducible expression of three defense genes 26 , which led the authors to conclude that Pep-13 induces immunity in a SERK3/BAK1-independent manner. Our data do not support this conclusion, since Pep-13 neither induces ROS formation, nor activates MAPK in StSERK3A/B -depleted plants.…”

Section: Discussionsupporting

confidence: 89%

Early Pep-13-induced immune responses are SERK3A/B-dependent in potato

Nietzschmann

Gorzolka

Smolka

et al. 2019

Sci Rep

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Potato plants treated with the pathogen-associated molecular pattern Pep-13 mount salicylic acid- and jasmonic acid-dependent defense responses, leading to enhanced resistance against Phytophthora infestans, the causal agent of late blight disease. Recognition of Pep-13 is assumed to occur by binding to a yet unknown plasma membrane-localized receptor kinase. The potato genes annotated to encode the co-receptor BAK1, StSERK3A and StSERK3B, are activated in response to Pep-13 treatment. Transgenic RNAi-potato plants with reduced expression of both SERK3A and SERK3B were generated. In response to Pep-13 treatment, the formation of reactive oxygen species and MAP kinase activation, observed in wild type plants, is highly reduced in StSERK3A/B-RNAi plants, suggesting that StSERK3A/B are required for perception of Pep-13 in potato. In contrast, defense gene expression is induced by Pep-13 in both control and StSERK3A/B-depleted plants. Altered morphology of StSERK3A/B-RNAi plants correlates with major shifts in metabolism, as determined by untargeted metabolite profiling. Enhanced levels of hydroxycinnamic acid amides, typical phytoalexins of potato, in StSERK3A/B-RNAi plants are accompanied by significantly decreased levels of flavonoids and steroidal glycoalkaloids. Thus, altered metabolism in StSERK3A/B-RNAi plants correlates with the ability of StSERK3A/B-depleted plants to mount defense, despite highly decreased early immune responses.

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Section: Discussionsupporting

confidence: 89%

Early Pep-13-induced immune responses are SERK3A/B-dependent in potato

Nietzschmann

Gorzolka

Smolka

et al. 2019

Sci Rep

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“…Recently, CERK1, an Arabidopsis fungal chitin receptor was reported to bind with synthetic β-1,3-glucan oligosaccharides that are present in both oomycete and fungi. Just like chitin perception via CERK1 (Wang H. et al, 2019), BAK1 was not found involved in this β-1,3-glucan-CERK1 induced PTI responses. Also, the cerk1 mutants showed higher susceptibility to a biotrophic oomycete H. arabidopsidis (Mélida et al, 2018).…”

Section: Cognate Prrs and Pamps Perception Modelsmentioning

confidence: 87%

“…are perceived in BAK1/SERK3 dependent manner. However, recently it was reported that unlike all known oomycetes PAMPs, perception of Pep-13 is not implicated through BAK1/SERK3 (Wang H. et al, 2019). Pep-13 has been shown to bind to a 100 kD monomeric integral plasma membrane receptor of parsley (Nennstiel et al, 1998;Blume et al, 2000) but its cognate PRR in other plant species is not yet known.…”

Section: Cognate Prrs and Pamps Perception Modelsmentioning

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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“…Pathogen effectors are thought to interfere with the PTI of the host, promoting colonization by the pathogen. PTI is induced by pathogen-associated molecular patterns (PAMPs), such as flagellin (or its derivative flg22) and EF-Tu from some bacterial pathogens and INF1 and XEG1 from oomycete pathogens (Gómez-Gómez and Boller, 2000;Zipfel et al, 2006;Du et al, 2015;Ma et al, 2015;Wang et al, 2019). Moreover, plant-derived molecular patterns, known as damageassociated molecular patterns (DAMPs), such as plant elicitor peptides (Peps), also elicit immune responses similar to those of PTI (Bigeard et al, 2015).…”

Section: Pvcrn35mentioning

confidence: 99%

Characterization of CRN-Like Genes From Plasmopara viticola: Searching for the Most Virulent Ones

et al. 2021

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Grapevine downy mildew is an insurmountable disease that endangers grapevine production and the wine industry worldwide. The causal agent of the disease is the obligate biotrophic oomycete Plasmopara viticola, for which the pathogenic mechanism remains largely unknown. Crinkling and necrosis proteins (CRN) are an ancient class of effectors utilized by pathogens, including oomycetes, that interfere with host plant defense reactions. In this study, 27 CRN-like genes were cloned from the P. viticola isolate YL genome, hereafter referred to as PvCRN genes, and characterized in silico and in planta. PvCRN genes in ‘YL’ share high sequence identities with their ortholog genes in the other three previously sequenced P. viticola isolates. Sequence divergence among the genes in the PvCRN family indicates that different PvCRN genes have different roles. Phylogenetic analysis of the PvCRN and the CRN proteins encoded by genes in the P. halstedii genome suggests that various functions might have been acquired by the CRN superfamily through independent evolution of Plasmopara species. When transiently expressed in plant cells, the PvCRN protein family shows multiple subcellular localizations. None of the cloned PvCRN proteins induced hypersensitive response (HR)-like cell death on the downy mildew-resistant grapevine Vitis riparia. This was in accordance with the result that most PvCRN proteins, except PvCRN11, failed to induce necrosis in Nicotiana benthamiana. Pattern-triggered immunity (PTI) induced by INF1 was hampered by several PvCRN proteins. In addition, 15 PvCRN proteins prevented Bax-induced plant programmed cell death. Among the cell death-suppressing members, PvCRN17, PvCRN20, and PvCRN23 were found to promote the susceptibility of N. benthamiana to Phytophthora capsici, which is a semi-biotrophic oomycete. Moreover, the nucleus-targeting member, PvCRN19, promoted the susceptibility of N. benthamiana to P. capsici. Therefore, these PvCRN proteins were estimated to be virulent effectors involved in the pathogenicity of P. viticola YL. Collectively, this study provides comprehensive insight into the CRN effector repertoire of P. viticola YL, which will help further elucidate the molecular mechanisms of the pathogenesis of grapevine downy mildew.

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The oomycete microbe-associated molecular pattern Pep-13 triggers SERK3/BAK1-independent plant immunity

Abstract: Key message Oomycetes MAMP Pep-13 can trigger SERK3/BAK1-independent PTI. Silencing of SERK3/BAK1 in solanaceous plants resulted in reduced expression of brassinosteroid marker genes and enhanced PTI transcriptional responses to Pep-13 treatment.

Cited by 13 publications

References 45 publications

Early Pep-13-induced immune responses are SERK3A/B-dependent in potato

Early Pep-13-induced immune responses are SERK3A/B-dependent in potato

The PTI to ETI Continuum in Phytophthora-Plant Interactions

Characterization of CRN-Like Genes From Plasmopara viticola: Searching for the Most Virulent Ones

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