白念珠菌是临床极为重要的条件性致病真菌，探索该病原菌毒力相关因子及致病机制具有重要意义。自噬作为真核细胞关键的自我消化机制，通过维持细胞稳态，在压力耐受、细胞分化、发育、衰老、信号转导等过程中扮演重要角色。然而，自噬在白念珠菌生理代谢尤其是细胞稳态维持中的功能尚有待深入研究。本项目首次系统开展白念珠菌自噬相关基因的功能研究，通过构建自噬报告系统、线粒体功能缺陷模型、内质网压力报告系统、核物质转运缺陷模型等，探索自噬在白念珠菌线粒体功能维持、内质网压力应答、核物质稳态维持及细胞周期调控中的作用，以及自噬在该病原菌压力耐受与致病过程中的功能。本项目旨在明确白念珠菌自噬与环境压力应答之间的相互关系，丰富自噬在白念珠菌细胞稳态维持方面的理论，同时发掘针对该病原菌的新型药物靶点，为临床治疗白念珠菌感染提供理论依据。

Candida albicans is one of the most important opportunistic pathogens in clinic. It is of significance to investigate the virulence-related factors and pathogenicity mechanisms in this pathogen. Autophagy is the key process of self-digestion in eukaryotic cells, playing essential roles in cellular homeostasis, stress tolerance, cellular differentiation, development, aging and signal transduction. However, the role of autophagy in C. albicans remains to be detailed. This study for the first time systematically investigates the functions of autophagy-related genes. By constructing the autophagy-reporting system, the mitochondrial fuction defect model, the endoplasmic reticulum (ER) stress-reporting system and the nucleus transport defect model, this study explores in detail the roles of autophagy in mitochondrial function maintenance, ER stress response, nucleus homeostasis maintenance, cell cycle regulation and pathogenicity of C. albicans. This study aims to uncover the connection between autophagy and stress response response, to shed novel light on the role of autophagy in cellular homeostasis maintenance, and to discover new drug targets against C. albicans-related infections.