灰霉菌是一种可侵染多种采后水果和蔬菜导致灰霉病害的模式病原真菌，对其致病性和调控机制的研究具有重要的理论和实践意义。黑色素是广泛存在于各种生物体内的多酚类聚合物，已被证明是多种植物病原真菌的一种重要致病因子，缺失黑色素会引起致病力下降或丧失。本项目在前期研究中发现，灰霉菌黑色素合成相关基因Bcpks13和Bcbrn1缺失突变后，对多种果蔬的致病力却极显著地增加，预示着黑色素的功能有待于在植物病原真菌中进行重新解读。本研究在前期工作基础上，拟采用分子遗传学、细胞学、生物化学、以及转录组学等手段，研究灰霉菌黑色素的生物合成代谢途径相关基因（Bcpks13，Bcbrn1，Bcscd1）对灰霉菌致病性的影响，探究它们在灰霉菌与寄主果实互作过程的作用机制，揭示黑色素的合成代谢在坏死营养型病原真菌致病过程中的特殊功能，为研究果蔬采后病害的控制靶点提供新思路。

Botrytis cinerea is a necrotrophic pathogen with a broad host range, causing gray mold disease and huge losses worldwide annually. It’s of greatly theoretical and practical value to investigate the pathogenicity and related regulation mechanism of this model pathogenic fungus. Melanin pigments are polymers ubiquitously formed by oxidative polymerization of phenolic or indolic compounds that is found in all biological kingdoms. Melanin has been recognized as a pathogenicity factor in several plant fungal pathogens, in which albino mutants have shown deficient or attenuated pathogenicity. However, our preliminary work on B. cinerea resulted in quite different principles. Knock-out mutation of two melanin biosynthetic genes in B. cinerea, the Bcpks13 and Bcbrn1, caused significant increase in pathogenicity of this pathogen on various fruits and vegetable, suggesting an unrevealed regulating mechanism of melanin biosynthesis for fungal pathogenicity. In this project, molecular genetics, cytology, biochemistry, and transcriptome analysis will be used to further investigate the particular roles of melanin synthesis genes (Bcpks13, Bcbrn1, and Bcscd1) in B. cinerea, and its correlation with expression of pathogenic factors and interaction with host plants will also be elucidated. The prospective results of this study aims to lay theoretical foundations for developing new targets of postharvest disease control.