It is revealed that CfMBZ1 plays a critical role in the pathogenesis of Glomerella leaf spot caused by C. fructicola and regulates appressorium-mediated penetration by modulating genes involved in peroxisome biogenesis, lipid droplet metabolism, and other penetration-related pathways.
Abstract
Colletotrichum fructicola, the primary causal agent of Glomerella leaf spot (GLS), is a destructive fungal pathogen of apple, whose underlying pathogenic mechanisms remain largely unknown. A previous transcriptomic analysis of infected leaves indicated induction of the transcription factor CfMBZ1. This study confirmed that CfMBZ1 is highly expressed in conidia and during early infection. To elucidate its function, we generated a ΔCfMBZ1 deletion mutant via homologous recombination. Phenotypic analysis revealed that ΔCfMBZ1 lost pathogenicity on apple leaves due to a blockage in appressorium-mediated host penetration, despite retaining the ability to form penetration pegs on cellophane. However, extension of invasive hyphae and necrotrophic growth in wounded apple fruit were unaffected. The mutant also exhibited defects in maintaining the integrity of the cell wall and cell membrane, as well as in tolerating oxidative and acid–base stress. Comparative transcriptome analysis suggested that CfMBZ1 regulates appressorium-mediated penetration by modulating genes involved in peroxisome biogenesis, lipid droplet metabolism, and other penetration-related pathways. Our findings reveal that CfMBZ1 plays a critical role in the pathogenesis of Glomerella leaf spot caused by C. fructicola.
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