Interaction between plant hormones in response to Botrytis cinerea infection in cut flowers with differential tissue sensitivity to ethylene

Abstract

Botrytis cinerea (B. cinerea), a major postharvest disease-causing fungus, causes considerable ornamental and economic losses in cut flowers, but the mechanisms by which phytohormones modulate B. cinerea resistance in cut flowers remain unclear. Here, we explored the role of plant hormones including ethylene (ETH), jasmonic acid (JA), and salicylic acid (SA), in the response to B. cinerea infection in rose cultivars with different ETH sensitivities. The results showed that ETH-highly sensitive (EthHS) cultivars exhibited faster disease progression and more severe symptoms of gray mold disease (GMD) symptoms than ETH-low sensitive (EthLS) cultivars when exposed to B. cinerea and ETH. B. cinerea infection significantly altered the expression patterns of ETH, JA, and SA biosynthesis and the signaling genes in rose petals. Notably, the activation of ETH- and SA-related genes by the GMD infection was closely related to the ETH sensitivity of the petal tissues, while JA signaling functioned independently. ETH and SA treatments increased the GMD susceptibility by upregulating B. cinerea histidine kinase receptors and pathogenicity-related genes, thereby accelerating tissue senescence in EthHS roses with or without B. cinerea infection. Contrastingly, the EthLS flowers treated with ETH and SA showed elevated GMD symptoms only when inoculated with fungi. Methyl JA (MeJA) treatment reduced the GMD severity and downregulated the transcription of B. cinerea-related genes, regardless of the tissue sensitivity to ETH. A working model was established to illustrate the antagonistic roles of ETH and SA against JA in regulating B. cinerea resistance in cut roses. These insights into hormone crosstalk provide potential strategies for enhancing B. cinerea resistance in cut rose flowers.