Alterations in sucrose and phenylpropanoid metabolism affected by BABA-primed defense in postharvest grapes and the associated transcriptional mechanism.

Defense elicitors can induce fruit disease resistance to control postharvest decay but may incur quality impairment. Our present work aimed to investigate the resistance against Botrytis cinerea induced by the elicitor β-aminobutyric acid (BABA) and to elucidate the specific transcriptional mechanism implicated in defense-related metabolic regulations. The functional dissection results demonstrated that after inoculation with the fungal necrotroph B. cinerea, a suite of critical genes encoding enzymes related to sucrose metabolism and phenylpropanoid pathway in priming defense in grapes were transcriptionally induced by 10 mM BABA treatment. In contrast, more UDP-glucose, a shared precursor of phenylpropanoid and sucrose metabolism, may be redirected to the phenylpropanoid pathway for the synthesis of phytoalexins, including trans-resveratrol and e-viniferin, in 100 mM BABA-treated grapes, resulting in direct resistance but compromised soluble sugar contents. An R2R3-type MYB protein from Vitis vinifera, VvMYB44, was isolated and characterized. VvMYB44 expression was significantly induced upon the grapes expressed defensive reaction. Subcellular localization, Y2H and Co-IP assays revealed that the nuclear-localized VvMYB44 physically interacted with the SA-responsive transcription co-activator NPR1 in vivo for defence expression. In addition, VvMYB44 directly bound to the promoter regions of sucrose and phenylpropanoid metabolism-related genes and transactivate their expression, thus tipping the balance of antifungal compound accumulation and soluble sugar maintenance. Hence, these results suggest that 2R-type VvMYB44 might be a potential positive participant in BABA-induced priming defense in grape berries, contributing to avoiding the excessive consumption of soluble sugars during the postharvest storage.