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Botrytis cinerea is a necrotrophic filamentous fungus that serves as a significant pathogen for over 1,400 plant species, causing the devastating disease known as gray mold. It is characterized by its ability to secrete a wide array of cell wall-degrading enzymes and reactive oxygen species (ROS) that trigger host cell death, allowing the fungus to feed on decomposing plant tissue [1, 2]. While it is primarily an agricultural concern affecting high-value crops like grapes, strawberries, and tomatoes, it also plays a dual role in viticulture by causing 'noble rot' under specific environmental conditions, which is essential for the production of certain dessert wines [3]. In human health, B. cinerea is recognized as a potent allergen and is the causative agent of 'winegrower's lung,' a form of hypersensitivity pneumonitis triggered by the inhalation of high concentrations of fungal spores [4]. From a pharmacological perspective, B. cinerea is not a single molecular target but rather a target organism for various classes of fungicides. Current chemical management strategies target specific fungal proteins and pathways, such as the succinate dehydrogenase complex (SDHIs), MAP kinases, and sterol biosynthesis enzymes [2, 5]. However, the fungus is notorious for its high genetic plasticity and rapid development of multi-drug resistance (MDR), often mediated by the overexpression of efflux transporters or point mutations in target genes. This high resistance profile presents a significant challenge for long-term agricultural disease control and necessitates the development of novel anti-fungal strategies [5, 6].
Inhibition of mitochondrial respiration (SDHIs), disruption of osmotic signal transduction, inhibition of methionine biosynthesis, inhibition of sterol biosynthesis (C-3 demethylase), and interference with microtubule assembly.
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