Manna A C, Bayer M G, Cheung A L
Laboratory of Bacterial Pathogenesis and Immunology, The Rockefeller University, New York, New York 10021, USA.
J Bacteriol. 1998 Aug;180(15):3828-36. doi: 10.1128/JB.180.15.3828-3836.1998.
The expression of extracellular virulence determinants in Staphylococcus aureus is controlled by a 510-nucleotide RNA molecule (RNAIII) which is a part of the agr system. The agr operon, which encodes a multicomponent signal transduction system, is partially under the influence of an unlinked regulatory locus called sar. The sar locus is composed of three overlapping transcripts, designated sarA (0.56 kb), sarC (0.8 kb), and sarB (1.2 kb), originating from the P1, P3, and P2 promoters, respectively. In this study, we analyzed the differential expression of these promoters by using transcriptional fusion with the xylE reporter gene to study the activation of the sar locus. The data confirm the existence of three independent promoters with different promoter activities. Maximal promoter activity was observed with the combined fusion of P2-P3-P1 promoters. Expression studies with a sigB mutant revealed that the P3 promoter is SigB dependent. Analysis of these transcriptional fusions in a sarA mutant and in complemented strains with each of the sar transcriptional units revealed that the sar locus is autoregulatory, with SarA acting as a positive regulator. From various transcriptional fusion studies of the upstream region of the P1 promoter, we have localized a 34-bp sequence which seems to play a role in down-modulating P1 transcription. Using heparin-Sepharose and DNA-specific columns, we partially purified a 12-kDa protein, possibly a repressor, which binds to the promoter regions upstream of P2 and P1 and which also binds to the 34-bp sequence. These data indicated that the regulation of the sar locus is complex and may involve the sar gene product(s) and other regulatory protein(s).
金黄色葡萄球菌细胞外毒力决定因素的表达受一个510个核苷酸的RNA分子(RNAIII)控制,该分子是agr系统的一部分。agr操纵子编码一个多组分信号转导系统,部分受一个名为sar的不连锁调控位点的影响。sar位点由三个重叠转录本组成,分别命名为sarA(0.56 kb)、sarC(0.8 kb)和sarB(1.2 kb),它们分别起源于P1、P3和P2启动子。在本研究中,我们通过与xylE报告基因进行转录融合来分析这些启动子的差异表达,以研究sar位点的激活情况。数据证实存在三个具有不同启动子活性的独立启动子。在P2 - P3 - P1启动子的联合融合中观察到最大启动子活性。对sigB突变体的表达研究表明,P3启动子依赖于SigB。在sarA突变体和用每个sar转录单元互补的菌株中对这些转录融合的分析表明,sar位点是自我调节的,SarA作为正调节因子起作用。通过对P1启动子上游区域的各种转录融合研究,我们定位了一个34 bp的序列,该序列似乎在下调P1转录中起作用。使用肝素 - 琼脂糖和DNA特异性柱,我们部分纯化了一种12 kDa的蛋白质,可能是一种阻遏物,它与P2和P1上游的启动子区域结合,也与34 bp序列结合。这些数据表明,sar位点的调控是复杂的,可能涉及sar基因产物和其他调控蛋白。