Analyses of sigma factor 28 of C. trachomatis

描述（由申请人提供）：沙眼衣原体是细菌性性传播感染的主要原因。这种重要病原体的基因表达调控尚未得到很好的理解。我们的长期目标是调查允许C.沙眼衣原体在不同的条件下生存，以及在宿主中持续存在并导致人类疾病。 我们证明了C.沙眼衣原体交替σ因子σ 28对热休克有反应，并识别衣原体的hctB启动子以及大肠杆菌的fliC启动子。这表明sigma 28可能参与了一组基因的转录，这是适应反应所必需的，使发育周期的成功完成。本提案的目的是了解衣原体sigma因子之一sigma 28的生物学功能，并描述其调节因子的特征。本研究的主要目的有两个：1）在C.沙眼我们还将检查这些启动子及其相关靶基因在与衣原体生理相关的条件下的活性; 2）我们将鉴定并表征衣原体中sigma 28的推定调节子，并检查sigma 28与其推定调节子之间的相互作用对sigma 28特异性转录的影响。从这些研究中获得的信息可能会导致更好地了解基因的整体调控，细胞内寄生，毒力，免疫逃避和持久性的C。沙眼

DESCRIPTION (provided by applicant): Chlamydia trachomatis is a major cause of bacterial sexually transmitted infections. The regulation of gene expression in this important pathogen has not been well understood. Our long-range goals are to investigate the global regulatory mechanisms that allow C. trachomatis to survive in different conditions, as well as to persist in the host and contribute to human disease. We have demonstrated that the C. trachomatis alternative sigma factor, sigma 28, responds to heat shock and recognizes the hctB promoter of Chlamydia and also the fliC promoter of Escherichia coli. This suggests that sigma28 may be involved in transcription of a group of genes, which are required for an adaptation response enabling the successful completion of the developmental cycle. The objective of this proposal is to understand the biological function of one of the chlamydial sigma factors, sigma28, and to characterize its regulator(s). We propose two specific aims: 1) We will identify and characterize sigma28-dependent promoters and the sigma28 regulated target genes in C. trachomatis. We will also examine the activities of these promoters and their related target genes under conditions that are physiologically relevant for Chlamydia and 2) We will identify and characterize the putative regulator(s) of sigma28 in Chlamydia, and examine the effect on sigma28 specific transcription of interactions between sigma28 and its putative regulators. Information derived from these studies may lead to a better understanding of global regulation of genes, intracellular parasitism, virulence, immune evasion and persistence of C. trachomatis.