Porphyromonas gingivalis, the causative agent of adult periodontitis, must gain resistance to frequent oxidative and nitric oxide (NO) stress attacks from immune cells in the periodontal pocket to survive. Previously, we found that, in the wild-type and under NO stress, the expression of PG1237 (CdhR), the gene encoding for a putative LuxR transcriptional regulator previously called community development and hemin regulator (CdhR), was upregulated 7.7-fold, and its adjacent gene PG1236 11.9-fold. Isogenic mutants P. gingivalis FLL457 (ΔCdhR::ermF), FLL458 (ΔPG1236::ermF), and FLL459 (ΔPG1236-CdhR::ermF) were made by allelic exchange mutagenesis to determine the involvement of these genes in P. gingivalis W83 NO stress resistance. The mutants were black pigmented and β hemolytic and their gingipain activities varied with strains. FLL457 and FLL459 mutants were more sensitive to NO compared to the wild type, and complementation restored NO sensitivity to that of the wild type. DNA microarray analysis of FLL457 showed that approximately 2% of the genes were upregulated and over 1% of the genes downregulated under NO stress conditions compared to the wild type. Transcriptome analysis of FLL458 and FLL459 under NO stress showed differences in their modulation patterns. Some similarities were also noticed between all mutants. The PG1236-CdhR gene cluster revealed increased expression under NO stress and may be part of the same transcriptional unit. Recombinant CdhR showed binding activity to the predicted promoter regions of PG1459 and PG0495. Taken together, the data indicate that CdhR may play a role in NO stress resistance and be involved in a regulatory network in P. gingivalis.

中文翻译：

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一氧化氮应激过程中牙龈卟啉单胞菌中 CdhR 的参与

牙龈卟啉单胞菌是成人牙周炎的病原体，必须抵抗牙周袋中免疫细胞频繁的氧化和一氧化氮 (NO) 应激攻击才能生存。此前，我们发现，在野生型和 NO 胁迫下，PG1237 ( CdhR ) 的表达上调了 7.7 倍，PG1237 ( CdhR ) 是编码假定的 LuxR 转录调节因子的基因，以前称为群落发育和氯高铁血红素调节因子 (CdhR)。及其邻近基因PG1236的11.9倍。同基因突变体牙龈卟啉单胞菌FLL457 (Δ CdhR :: ermF )、FLL458 (Δ PG1236 :: ermF ) 和 FLL459 (Δ PG1236-CdhR:: ermF ) 是通过等位基因交换诱变产生的，以确定这些基因在牙龈卟啉单胞菌 W83 NO 胁迫抗性中的参与。突变体呈黑色，具有β溶血性，其牙龈蛋白酶活性因菌株而异。与野生型相比，FLL457和FLL459突变体对NO更敏感，并且互补将NO敏感性恢复到野生型。FLL457的DNA微阵列分析显示，与野生型相比，在NO胁迫条件下，大约2%的基因上调，超过1%的基因下调。NO 胁迫下 FLL458 和 FLL459 的转录组分析显示它们的调制模式存在差异。所有突变体之间也发现了一些相似之处。PG1236 -CdhR基因簇显示在 NO 胁迫下表达增加，并且可能是同一转录单位的一部分。重组 CdhR 显示出与PG1459和PG0495的预测启动子区域的结合活性。综上所述，数据表明 CdhR 可能在 NO 应激抵抗中发挥作用，并参与牙龈卟啉单胞菌的调节网络。