ArticlePlanta2019
The elicitin β-cryptogein's activity in tomato is mediated by jasmonic acid and ethylene signalling pathways independently of elicitin-sterol interactions.
Article in Planta, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
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Who cites it
8 citing papers in PubMed, 19 citations in OpenAlex.
- Review
- The function of plant PR1 and other members of the CAP protein superfamily in plant-pathogen interactions.Molecular plant pathology · 2023Review
- Characteristics, Roles and Applications of Proteinaceous Elicitors from Pathogens in Plant Immunity.Life (Basel, Switzerland) · 2023Review
- Unraveling Plant Cell Death duringMicroorganisms · 2022Review
- Small G Protein StRab5b positively regulates potato resistance toFrontiers in plant science · 2022Article
- Article
- Silencing of phosphoinositide dependent protein kinase orthologs reduces hypersensitive cell death inPlant biotechnology (Tokyo, Japan) · 2020Article
- Apoplastic Cell Death-Inducing Proteins of Filamentous Plant Pathogens: Roles in Plant-Pathogen Interactions.Frontiers in genetics · 2020Review
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
Abstract
MAIN
conclusionThe level of resistance induced in different tomato genotypes after β-CRY treatment correlated with the upregulation of defence genes, but not sterol binding and involved ethylene and jasmonic acid signalling. Elicitins, a family of small proteins secreted by Phytophthora and Pythium spp., are the most well-known microbe-associated molecular patterns of oomycetes, a lineage of fungus-like organisms that include many economically significant crop pathogens. The responses of tomato plants to elicitin INF1 produced by Phytophthora infestans have been studied extensively. Here, we present studies on the responses of three tomato genotypes to β-cryptogein (β-CRY), a potent elicitin secreted by Phytophthora cryptogea that induces hypersensitive response (HR) cell death in tobacco plants and confers greater resistance to oomycete infection than acidic elicitins like INF1. We also studied β-CRY mutants impaired in sterol binding (Val84Phe) and interaction with the binding site on tobacco plasma membrane (Leu41Phe), because sterol binding was suggested to be important in INF1-induced resistance. Treatment with β-CRY or the Val84Phe mutant induced resistance to powdery mildew caused by the pathogen Pseudoidium neolycopersici, but not the HR cell death observed in tobacco and potato plants. The level of resistance induced in different tomato genotypes correlated with the upregulation of defence genes including defensins, β-1,3-glucanases, heveins, chitinases, osmotins, and PR1 proteins. Treatment with the Leu41Phe mutant did not induce this upregulation, suggesting similar elicitin recognition in tomato and tobacco. However, here β-CRY activated ethylene and jasmonic acid signalling, but not salicylic acid signalling, demonstrating that elicitins activate different downstream signalling processes in different plant species. This could potentially be exploited to enhance the resistance of Phytophthora-susceptible crops.
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