Aggregatibacter actinomycetemcomitans is a gram-negative bacterium associated with periodontal disease and a variety of disseminated extra-oral infections. Tissue colonization is mediated by fimbriae and non-fimbriae adhesins resulting in the formation of a sessile bacterial community or biofilm, which confers enhanced resistance to antibiotics and mechanical removal. The environmental changes experienced by A. actinomycetemcomitans during infection are detected and processed by undefined signaling pathways that alter gene expression. In this study, we have characterized the promoter region of the extracellular matrix protein adhesin A (EmaA), which is an important surface adhesin in biofilm biogenesis and disease initiation using a series of deletion constructs consisting of the emaA intergenic region and a promotor-less lacZ sequence. Two regions of the promoter sequence were found to regulate gene transcription and in silico analysis indicated the presence of multiple transcriptional regulatory binding sequences. Analysis of four regulatory elements, CpxR, ArcA, OxyR, and DeoR, was undertaken in this study. Inactivation of arcA, the regulator moiety of the ArcAB two-component signaling pathway involved in redox homeostasis, resulted in a decrease in EmaA synthesis and biofilm formation. Analysis of the promoter sequences of other adhesins identified binding sequences for the same regulatory proteins, which suggests that these proteins are involved in the coordinate regulation of adhesins required for colonization and pathogenesis.

中文翻译：

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Aggregatibacter actinomycetemcomitans 粘附素合成的调控

Aggregatibacter actinomycetemcomitans是一种与牙周病和各种播散性口腔外感染相关的革兰氏阴性细菌。组织定植由菌毛和非菌毛粘附素介导，导致形成无柄细菌群落或生物膜，从而增强对抗生素和机械去除的抵抗力。A经历的环境变化。放线菌伴生菌在感染期间，通过改变基因表达的未定义信号通路检测和处理。在这项研究中，我们描述了细胞外基质蛋白粘附素 A (EmaA) 的启动子区域，它是生物膜生物发生和疾病启动中的重要表面粘附素，使用一系列由 emaA 基因间区域和无启动子组成的缺失构建体lacZ序列。发现启动子序列的两个区域可以调节基因转录，计算机分析表明存在多个转录调节结合序列。本研究对四种调节元素 CpxR、ArcA、OxyR 和 DeoR 进行了分析。arcA失活，参与氧化还原稳态的 ArcAB 双组分信号通路的调节部分导致 EmaA 合成和生物膜形成减少。对其他粘附素的启动子序列的分析确定了相同调节蛋白的结合序列，这表明这些蛋白质参与了定植和发病机制所需的粘附素的协调调节。