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.