Integrated Transcriptomic, Enzymatic, and Immunolocalization Analysis Reveals Pectin Remodeling-Mediated Defense Against Fusarium oxysporum f. sp. cubense Race 4 in Banana
TL;DR
Findings establish pectin degradation-mediated immunity as a resistance mechanism in banana and provide potential targets for Fusarium wilt resistance breeding.
Abstract
Fusariumoxysporum f. sp. cubense race 4 (Foc 4) causes Fusarium wilt by penetrating root cell walls, yet the molecular basis of cell wall-mediated resistance remains poorly understood. Here, we investigated the transcriptional, enzymatic, and cellular responses of the resistant banana cultivar Dongjiao No. 1 (DJ) and its susceptible mutant ke2 following Foc 4 infection. RNA sequencing revealed that DJ specifically upregulated a pectin degradation cassette comprising pectin methylesterase (PME3-Like), pectin acetylesterase (PAE1), and polygalacturonases (PG1, PG3, PG5, PG-Like-4) at the bud seedling stage. Immunolocalization further revealed robust, tissue-specific PME deployment, with stable abundance at the primary infection site and differential redistribution in aerial tissues. This enzymatic cascade degraded homogalacturonan, confirmed by the simultaneous loss of pectin epitopes recognized by JIM5 and JIM7 antibodies. Additionally, the upregulation of PTI1, MAPK cascades, calcium-dependent protein kinases (CDPK3, CML31), and respiratory burst oxidase homologs (RBOHs) was also observed in DJ. The differential transcription of salicylic acid signaling (TGA1–PR1), jasmonic acid derepression (TIFY/JAZ), and flavonoid phytoalexin biosynthesis in DJ further reinforced the defense response. In contrast, ke2 failed to activate the pectin degradation machinery, exhibited attenuated immune signaling, and retained intact pectin vulnerable to pathogen exploitation. These findings establish pectin degradation-mediated immunity as a resistance mechanism in banana and provide potential targets for Fusarium wilt resistance breeding.