全球每年侵袭性念珠菌病患者超过200万例，白色念珠菌（CA）因极易形成生物膜感染等特点，已成为念珠菌病中致病率和致死率最高的病原体。大量文献报道表明黏附是生物膜形成的关键因素，课题组已发现抑制或激动Sir2能够显著影响CA黏附进程，但Sir2对CA黏附的调控作用和机制还不清楚。因此我们假设：Sir2通过去乙酰化作用调控黏附关键因子Als3蛋白或基因水平影响CA黏附。本课题将运用基因芯片技术筛选Sir2调控的差异基因，结合筛选信息探讨Sir2对差异基因和转录因子Efg1、转录调节因子Ume6的调控作用，揭示黏附过程中Sir2对关键基因以及关键转录调控过程的影响，进而研究Sir2对黏附基因ALS3转录和蛋白表达的调控机制，明确Sir2对Als3的调控作用是否需要去乙酰化酶Rpd3、Hda1的协同作用，为进一步探索CA生物膜感染的分子生物学过程提供参考，为开发新的念珠菌病治疗策略提供实验依据。

Each year, there are more than 2 million cases of invasive candida infection all over the world, of which, Candida albicans (CA) becoming one of the highest morbidity and mortality of pathogens for easy to form a biofilm state infection. A large number of literatures reported that adhesion was the key factor of biofilm formation. Our research found that either inhibiting or activating Sir2 can significantly affect the CA adhesion process, but the regulation and mechanism of Sir2 on the adhesion process is not clear. Therefore, we hypothesized that Sir2 influences CA adhesion by deacetylation to regulate the protein or gene level of the adhesion key factor Als3. This project uses gene chip technology to screen the differentially expressed genes of Sir2 and to explore the regulatory role of Sir2 on differentially expressed genes and transcription factor Efg1 and transcriptional regulator Ume6 in combination with screening information to reveal the effects of Sir2 on key genes and transcriptional regulation during adhesion. To study the regulatory mechanism of Sir2 on the transcriptional and protein expression of adhesion gene ALS3 and find out whether the regulation of Sir2 on Als3 requires the synergistic effect of other sirtuins Rpd3 and Hda1. This project would provide further understanding of the molecular biology process of CA biofilm infection, and afford experimental evidence for the development of new treatment strategies of Candida.