耐辐射奇球菌群体感应调控因子DqsR参与氧化胁迫抗性基因调控的分子机制

耐辐射奇球菌（DR）是一种能够忍受强烈电离辐射、氧化剂等极端环境的微生物，氧化抗性体系在DR菌超强抗性中起着重要作用。申请人前期研究发现了DR菌特殊的DqsIR群体感应系统，其调控因子DqsR突变导致菌体氧化抗性显著降低和胞内氧化压力响应、损伤修复等抗性基因转录水平下调，表明DqsR可能是一种多效性调控因子。目前DqsR参与氧化胁迫抗性基因调控的分子机制尚不清楚。本课题计划在前期研究的基础上，通过基因突变与补偿、蛋白与信号分子相互作用、蛋白与DNA相互作用分析等手段，研究并揭示群体感应调控因子DqsR的信号结合作用特性、靶基因的调控和序列特征等分子机制，阐明DqsR对氧化胁迫抗性基因的调控规律，旨在从群体感应水平揭示耐辐射奇球菌应对氧化胁迫的抗性作用机制，为深入了解菌体极端环境抗性机理提供基础和新的见解。

Deinococcus radiodurans (DR) is a bacterium which is known for its resistance to extreme stresses including irradiation and oxidants. Intracellular oxidative-stress resistant system plays important roles in its exceptional resistance to stresses. Our previous results identified the special DqsIR quorum sensing system (QS) in D. radiodurans. Gene mutation of its regulator DqsR resulted in significant decrease of cellular resistance to oxidative stress and down-regulation of transcriptional level of resistant genes including intracellular oxidative-stress response and damage repair genes, indicating that DqsR might be a pleiotropic regulator. The molecular mechanism of gene regulation by DqsR on oxidative-stress resistant genes remains unclear. Based on our previous study, we plan to investigate the binding properties of DqsR with QS signals, gene regulation mechanism and conserved binding sites on targeted genes of DqsR using analyses including gene mutation and functional complementation, interactions of protein with signals and with DNA. The objectives of this project are to elucidate the regulation mechanism of DqsR on oxidative-stress resistant genes and reveal the resistance of D. radiodurans in response to oxidative stress in view of quorum sensing. The results will provide fundament and novel insights to understanding the resistance of D.radiodurans to extreme stresses.