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Monilinia fructicola is a filamentous ascomycete fungus and the primary causative agent of brown rot in stone fruits such as peaches, nectarines, cherries, and plums (EPPO Global Database, 2020). As a necrotrophic pathogen, it colonizes host tissues by secreting cell-wall-degrading enzymes and toxic metabolites, leading to blossom blight, twig cankers, and rapid fruit decay (Amiri et al., 2009). Although it is not a target for human therapeutic intervention, it is a major target for agricultural fungicides. These chemical agents typically aim to disrupt vital fungal processes, including the biosynthesis of ergosterol, mitochondrial respiration, and microtubule assembly (Hu et al., 2011). The high economic impact of M. fructicola is exacerbated by its ability to develop resistance to several classes of fungicides, which has prompted extensive research into its genome and the identification of specific molecular targets like sterol 14-alpha-demethylase and succinate dehydrogenase (Luo et al., 2010; Chen et al., 2013).
Fungicides targeting this organism work by inhibiting sterol 14-alpha-demethylase (DMIs), the cytochrome bc1 complex (QoIs), succinate dehydrogenase (SDHIs), or beta-tubulin assembly (benzimidazoles).
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