Glomerella leaf spot (GLS), mainly caused by Colletotrichum fructicola, is a destructive disease of apple. However, the underlying pathogenesis mechanisms of GLS are still largely obscure. Previous infection transcriptome analysis showed that transcription factor CfGti1 was induced during leaf infection. The present study confirms that the CfGti1 gene is strongly expressed in conidia and early infection. To identify functions performed, we generated gene deletion mutant ΔCfGti1 by homologous recombination. Phenotypic analysis revealed that ΔCfGti1 lost pathogenicity to apple leaves by blocking appressorium-mediated host penetration, although penetration pegs still developed on cellophane. In addition, ΔCfGti1 colonization and hyphal extension in wounded apple fruit were dramatically decreased. The ΔCfGti1 mutant exhibited defects in growth and development of hyphae, which may be partly responsible for its inability to colonize apple. Comparative transcriptome and qRT-PCR analyses suggested that CfGti1 regulated appressorium-mediated host penetration by modulating genes related to metabolism of appressorial lipid droplets. Interestingly, CfGti1 also regulated the expression of ybtS and AKT1 or AFT1-1 related to biosynthesis of AK and AF host-specific toxins. This study demonstrated that CfGti1 is a pivotal regulator for apple GLS pathogenesis in C. fructicola.

Parkinson’s disease (PD) is a neurodegenerative disease that is closely related to genetic and environmental factors, among which pesticide exposure is considered an important risk factor. Fresh jujube and hawthorn, as widely consumed fruits, may contain pesticide residues, but the potential effects of long-term low-dose intake on PD are not yet clear. This study combines network toxicology and molecular docking technology to elucidate the molecular mechanism of PD induced by residual pesticides in fresh jujube and hawthorn. Firstly, common risk pesticides (such as organophosphates and pyrethroids) in fresh jujube and hawthorn were screened through the database. Subsequently, a “pesticide target—PD” interactive network was constructed using network toxicology to predict key targets and related pathways. Finally, molecular docking technology was used to verify the binding ability of pesticide molecules to PD-related proteins. The results indicate that some pesticides (such as chlorpyrifos and cypermethrin) may increase the risk of PD by affecting lipid metabolism and oxidative stress response. This study provides a new approach for assessing the neurotoxicity of pesticide residues and suggests the need to pay attention to the potential impact of dietary pesticide exposure on PD, providing a scientific basis for food safety regulation and PD prevention strategies.

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 Δ CfMBZ1 deletion mutant via homologous recombination. Phenotypic analysis revealed that Δ CfMBZ1 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 .