有效利用寄主营养是病原微生物侵染和定殖宿主的先决条件。昆虫病原真菌主要通过穿透体壁侵染宿主，对昆虫体壁营养的利用能力与侵染致病性密切相关。申请人通过T-DNA插入突变发现，一个F-box蛋白Bbfrp1是调控球孢白僵菌利用昆虫体壁营养影响侵染致病的重要因子。缺失Bbfrp1削弱了菌株利用昆虫体壁的几丁质和蛋白质成分的能力，导致穿透昆虫体壁受阻，毒力显著下降。该发现为揭示病原真菌利用昆虫体壁营养引起侵染致病的调控机制提供了新线索。本项目拟通过F-box结构域缺失，探究Bbfrp1对病原真菌利用昆虫体壁营养的调控作用与泛素-蛋白酶体途径的关系，进而利用IP及MS等方法鉴定Bbfrp1的互作蛋白，解析互作机制及互作蛋白在球孢白僵菌利用昆虫体壁营养和侵染致病中的功能。项目的开展，将为揭示病原真菌通过掠夺寄主营养引起侵染致病的机理提供新的理论支撑，并为菌株遗传改良和高效真菌杀虫剂的研制提供科学依据。

Nutrition acquirement from host is an essential prerequisite for the onset and colonization of an infection by pathogenic microorganisms. Insect pathogenic fungi infect host via penetrating cuticle directly, the ability of nutrition assimilation from cuticle is closely related to their pathogenicity. An F-box protein Bbfrp1 was identified using T-DNA insertional mutagenesis, which is a crucial factor in regulating fungal penetration of insect cuticle via controlling nutrition acquirement from host in Beauveria bassiana. Deletion Bbfrp1 decreased chitin and protein assimilation, resulting in impaired penetration in B. bassiana. The results provide important clues to clarify the pathogenesis mechanism of nutrition acquirement from insect cuticle facilitating infection in insect pathogenic fungi. This project is committed to analysis the relationship between Bbfrp1 and ubiquitin-proteasome pathway in regulation nutrition acquirement from host using F-box domain deletion. Subsequently, IP and MS are used to identify the proteins interacted with Bbfrp1. The roles of target proteins of Bbfrp1 will be further explored in the fungal nutrition acquirement from insect cuticle and colonization. It will lead to uncover the mechanism of F-box protein Bbfrp1 regulating fungal penetration of insect cuticle via control of nutrition acquirement from host in B. bassiana. This project seeks to provide a new insight into the fungal pathogenesis in the aspect of nutrition acquirement from host and colonization. It could also give some clues in strain improvement and fungal insecticide development.