Gummosis, one of the most detrimental diseases to peach industry worldwide, can be induced by Lasiodiplodia theobromae. Ethylene (ET) is known to trigger gum exudates, but the mechanism underlying in fungus-induced gummosis still remains unclear. In this study, L. theobromae infection triggered the accumulations of ET and jasmonic acid (JA), but not salicylic acid (SA) in a susceptible peach variety. The 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, the 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 lesion size. ET treatment reduced JA level and the transcripts of the JA biosynthetic genes OPRs, but increased SA content and the expression of its biosynthetic genes PALs. Altogether, we suggest that endogenous and exogenous ET aggravate gummosis disease by transactivating the 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 orchestrates plant defense responses in peach during L. theobromae infection.
Integrated transcriptomic and metabolic analyses reveal that ethylene enhances peach susceptibility to Lasiodiplodia theobromae-induced gummosis
Francesca Cardinale;
2022-01-01
Abstract
Gummosis, one of the most detrimental diseases to peach industry worldwide, can be induced by Lasiodiplodia theobromae. Ethylene (ET) is known to trigger gum exudates, but the mechanism underlying in fungus-induced gummosis still remains unclear. In this study, L. theobromae infection triggered the accumulations of ET and jasmonic acid (JA), but not salicylic acid (SA) in a susceptible peach variety. The 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, the 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 lesion size. ET treatment reduced JA level and the transcripts of the JA biosynthetic genes OPRs, but increased SA content and the expression of its biosynthetic genes PALs. Altogether, we suggest that endogenous and exogenous ET aggravate gummosis disease by transactivating the 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 orchestrates plant defense responses in peach during L. theobromae infection.
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