ArticleHorticulture research2022
Integrated transcriptomic and metabolic analyses reveal that ethylene enhances peach susceptibility to Lasiodiplodia theobromae-induced gummosis.
Article in Horticulture research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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10 citing papers in PubMed, 26 citations in OpenAlex.
- Rhizosphere microbial shifts drive amygdalin detoxification and jasmonate-mediated alleviation of peach autotoxicity.The ISME journal · 2026Article
- Tea Plant miR5368-p5 Negatively Regulates Resistance Against Lasiodiplodia theobromae Through Targeting the CsWRKY57-CsLRR-RLK Module.Molecular plant pathology · 2025Article
- Infection mechanism of Botryosphaeria dothidea and the disease resistance strategies of Chinese hickory (Carya cathayensis).BMC plant biology · 2024Article
- Biocontrol of Peach Gummosis byJournal of microbiology and biotechnology · 2024Article
- Comparative transcriptome and metabolome analysis revealed diversity in the response of resistant and susceptible rose (Frontiers in plant science · 2024Article
- Transcriptomic and sugar metabolic analysis reveals molecular mechanisms of peach gummosis in response toFrontiers in plant science · 2024Article
- Two interacting ethylene response factors negatively regulate peach resistance to Lasiodiplodia theobromae.Plant physiology · 2023Article
- Repeated mechanical damage enhancedFrontiers in plant science · 2023Article
- Silicon inhibits gummosis by promoting polyamine synthesis and repressing ethylene biosynthesis in peach.Frontiers in plant science · 2022Article
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10 authors at 2 institutions in 2 countries.
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Abstract
Gummosis, one of the most detrimental diseases to the peach industry worldwide, can be induced by Lasiodiplodia theobromae. Ethylene (ET) is known to trigger the production of gum exudates, but the mechanism underlying fungus-induced gummosis remains unclear. In this study, L. theobromae infection triggered the accumulation of ET and jasmonic acid (JA) but not salicylic acid (SA) in a susceptible peach variety. Gaseous ET and its biosynthetic precursor increased gum formation, whereas ET inhibitors repressed it. SA and methyl-jasmonate treatments did not influence gum formation. RNA-seq analysis indicated that L. theobromae infection and ET treatment induced a shared subset of 1808 differentially expressed genes, which were enriched in the category "starch and sucrose, UDP-sugars metabolism". Metabolic and transcriptional profiling identified a pronounced role of ET in promoting the transformation of primary sugars (sucrose, fructose, and glucose) into UDP-sugars, which are substrates of gum polysaccharide biosynthesis. Furthermore, ethylene insensitive3-like1 (EIL1), a key transcription factor in the ET pathway, could directly target the promoters of the UDP-sugar biosynthetic genes UXS1a, UXE, RGP and MPI and activate their transcription, as revealed by firefly luciferase and yeast one-hybrid assays. On the other hand, the supply of SA and inhibitors of ET and JA decreased the lesion size. ET treatment reduced JA levels and the transcription of the JA biosynthetic gene OPR but increased the SA content and the expression of its biosynthetic gene PAL. Overall, we suggest that endogenous and exogenous ET aggravate gummosis disease by transactivating UDP-sugar metabolic genes through EIL1 and modulating JA and SA biosynthesis in L. theobromae-infected peach shoots. Our findings shed light on the molecular mechanism by which ET regulates plant defense responses in peach during L. theobromae infection.
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