ArticleJournal of experimental botany2011
The involvement of jasmonates and ethylene in Alternaria alternata f. sp. lycopersici toxin-induced tomato cell death.
Article in Journal of experimental botany, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 53 citations in OpenAlex.
- Alternaria diseases on potato and tomato.Molecular plant pathology · 2024Review
- Jasmonic acid contributes to rice resistance against Magnaporthe oryzae.BMC plant biology · 2022Article
- The Core Jasmonic Acid-Signalling ModuleCurrent issues in molecular biology · 2022Article
- Recent Advances inJournal of fungi (Basel, Switzerland) · 2022Review
- Leaf herbivory counteracts nematode-triggered repression of jasmonate-related defenses in tomato roots.Plant physiology · 2021Article
- Sphinganine-Analog Mycotoxins (SAMs): Chemical Structures, Bioactivities, and Genetic Controls.Journal of fungi (Basel, Switzerland) · 2020Review
- Overexpression of FBR41 enhances resistance to sphinganine analog mycotoxin-induced cell death and Alternaria stem canker in tomato.Plant biotechnology journal · 2020Article
- (Horticulture research · 2020Article
- A Disease Resistance Elicitor Laminarin Enhances Tea Defense against a Piercing Herbivore Empoasca (Matsumurasca) onukii Matsuda.Scientific reports · 2019Article
- Biostimulatory activities of Ascophyllum nodosum extract in tomato and sweet pepper crops in a tropical environment.PloS one · 2019Article
- Review
- Review
- Desensitization of idiopathic pulmonary fibrosis fibroblasts to Alternaria alternata extract-mediated necrotic cell death.Physiological reports · 2016Article
- Critical Role of COI1-Dependent Jasmonate Pathway in AAL toxin induced PCD in Tomato Revealed by Comparative Proteomics.Scientific reports · 2016Article
- Modifications of Sphingolipid Content Affect Tolerance to Hemibiotrophic and Necrotrophic Pathogens by Modulating Plant Defense Responses in Arabidopsis.Plant physiology · 2015Article
- Tomato histone H2B monoubiquitination enzymes SlHUB1 and SlHUB2 contribute to disease resistance against Botrytis cinerea through modulating the balance between SA- and JA/ET-mediated signaling pathways.BMC plant biology · 2015Article
- Secondary metabolites in fungus-plant interactions.Frontiers in plant science · 2015Review
- An Arabidopsis mutant impaired in intracellular calcium elevation is sensitive to biotic and abiotic stress.BMC plant biology · 2014Article
- Perception, signaling and cross-talk of jasmonates and the seminal contributions of the Daoxin Xie's lab and the Chuanyou Li's lab.Plant cell reports · 2014Review
- Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Previous studies have shown that an ethylene (ET)-dependent pathway is involved in the cell death signalling triggered by Alternaria alternata f. sp. lycopersici (AAL) toxin in detached tomato (Solanum lycopersicum) leaves. In this study, the role of jasmonic acid (JA) signalling in programmed cell death (PCD) induced by AAL toxin was analysed using a 35S::prosystemin transgenic line (35S::prosys), a JA-deficient mutant spr2, and a JA-insensitive mutant jai1. The results indicated that JA biosynthesis and signalling play a positive role in the AAL toxin-induced PCD process. In addition, treatment with the exogenous ET action inhibitor silver thiosulphate (STS) greatly suppressed necrotic lesions in 35S::prosys leaves, although 35S::prosys leaflets co-treated with AAL toxin and STS still have a significant high relative conductivity. Application of 1-aminocyclopropane-1-carboxylic acid (ACC) markedly enhanced the sensitivity of spr2 and jai1 mutants to the toxin. However, compared with AAL toxin treatment alone, exogenous application of JA to the ET-insensitive mutant Never ripe (Nr) did not alter AAL toxin-induced cell death. In addition, the reduced ET-mediated gene expression in jai1 leaves was restored by co-treatment with ACC and AAL toxin. Furthermore, JA treatment restored the decreased expression of ET biosynthetic genes but not ET-responsive genes in the Nr mutant compared with the toxin treatment alone. Based on these results, it is proposed that both JA and ET promote the AAL toxin-induced cell death alone, and the JAI1 receptor-dependent JA pathway also acts upstream of ET biosynthesis in AAL toxin-triggered PCD.
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