To
explore the role of hexokinase (HXK) on disease resistance in
peach fruit, peaches were treated with N-acetyl-d-glucosamine (NAG), a known HXK inhibitor, and then inoculated
with Monilinia fructicola. We demonstrate
that NAG significantly inhibits HXK activity, which in turn results
in significantly reduced resistance to M. fructicola infection. In the HXK-inhibited fruit, the sucrose content was higher
and the glucose and fructose contents were lower than in the control
fruit. By transcriptome analysis, we found 347 differentially expressed
genes (DEGs) between NAG-treated and control peaches, most of which
were involved in the mitogen-activated protein kinase signaling pathway
in plants, plant–pathogen interaction, plant hormone signal
transduction, and the phenylpropanoid biosynthesis pathway. In particular,
the DEGs related to phenylpropanoid metabolism, such as peroxidase,
flavonoid, and isoflavonoid biosynthesis were significantly downregulated.
Nontargeted metabolomic analysis revealed 44 differential metabolites,
9 of which were increased and 35 of which were decreased in the NAG-treated
fruit. The decreased metabolites were secondary metabolites, including
polyphenols, flavonoids, terpenoids, and glycosides. The relationship
between HXK and phenylpropanoid metabolism was further investigated,
and we found that in HXK-inhibited fruits the activities of phenylalanine
ammonia-lyase, 4-coumarate-CoA ligase, and cinnamate 4-hydroxylase
were significantly decreased over the control fruit, as well as the
total phenol and total flavone contents were also significantly decreased.
These results demonstrate that the inhibition of HXK activity decreases
the disease resistance of peach fruits by affecting sugar metabolism
and the phenylpropanoid pathway.