Phenylpropanoid pathway mediated the defense response of ‘Korla’ fragrant pear against Alternaria alternata infection

Alternaria alternata has been found to be the dominating pathogenic fungus of harvested ‘Korla’ fragrant pear, and the resulting blackhead disease is a significant factor affecting the storage quality of pears. The present study explored the specific mechanisms by which the phenylpropanoid pathway mediates the defense response to A. alternata infection in pear fruit. In the A. alternata-inoculated group, the fruit exhibited increased activity and gene expression levels of key enzymes (PAL, C4H, and 4CL) as well as higher content of phenolic acids (trans-cinnamic acid, ferulic acid, caffeic acid, p-coumaric acid, and sinapic acid) and total phenol in the general phenylpropanoid pathway. In the mid-to-late storage period, the activity and gene expression levels of key enzymes in the lignin biosynthetic pathway (CCR and CAD) were suppressed, and the content of lignin monomers (sinapyl alcohol, coniferyl alcohol, and p-coumaryl alcohol) and lignin was reduced. Notably, the activity and gene expression levels of flavonoid biosynthetic pathway-related enzymes (CHS and CHI) as well as the content of various flavonoids (naringenin, apigenin, rutin, quercetin, and epicatechin) and total flavonoids continuously increased in response to A. alternata infection in the early to middle stages of storage but declined in the late storage period. In summary, the initial infection of A. alternata infection activated the stress response of pear fruit, particularly the phenylpropanoid–flavonoid branch pathway, to enhance the fruit’s defense against pathogens, but with the prolongation of the infestation time, the fruit could not continuously resist the invasion of pathogens, ultimately leading to the outbreak of disease. The present findings furnish a theoretical foundation further elucidating the interaction between ‘Korla’ fragrant pear and A. alternata and for developing an effective strategy to control the blackhead disease.