Camacho Eva M, Serna Ana, Madrid Cristina, Marqués Silvia, Fernández Raúl, de la Cruz Fernando, Juárez Antonio, Casadesús Josep
Departamento de Genética, Facultad de Biología, Universidad de Sevilla, Apartado 1095, E-41080 Sevilla, Spain.
J Bacteriol. 2005 Aug;187(16):5691-9. doi: 10.1128/JB.187.16.5691-5699.2005.
DNA adenine methylase (Dam(-)) mutants of Salmonella enterica serovar Typhimurium contain reduced levels of FinP RNA encoded on the virulence plasmid. Dam methylation appears to regulate finP transcription, rather than FinP RNA stability or turnover. The finP promoter includes canonical -10 and -35 modules and depends on the sigma(70) factor. Regulation of finP transcription by Dam methylation does not require DNA sequences upstream from the -35 module, indicating that Dam acts at the promoter itself or downstream. Unexpectedly, a GATC site overlapping with the -10 module is likewise dispensable for Dam-mediated regulation. These observations indicate that Dam methylation regulates finP transcription indirectly and suggest the involvement of a host factor(s) responsive to the Dam methylation state of the cell. We provide evidence that one such factor is the nucleoid protein H-NS, which acts as a repressor of finP transcription in a Dam(-) background. H-NS also restrains transcription of the overlapping traJ gene, albeit in a Dam-independent fashion. Hence, the decreased FinP RNA content found in Dam(-) hosts of S. enterica appears to result from H-NS-mediated repression of finP transcription.
鼠伤寒沙门氏菌血清型鼠伤寒杆菌的DNA腺嘌呤甲基化酶（Dam(-)）突变体中，毒力质粒上编码的FinP RNA水平降低。Dam甲基化似乎调节finP转录，而不是FinP RNA的稳定性或周转。finP启动子包括典型的-10和-35模块，并依赖于sigma(70)因子。Dam甲基化对finP转录的调节不需要-35模块上游的DNA序列，这表明Dam作用于启动子本身或下游。出乎意料的是，与-10模块重叠的GATC位点对于Dam介导的调节同样是可有可无的。这些观察结果表明，Dam甲基化间接调节finP转录，并提示存在一个对细胞Dam甲基化状态有反应的宿主因子。我们提供的证据表明，其中一个这样的因子是类核蛋白H-NS，它在Dam(-)背景下作为finP转录的阻遏物。H-NS也抑制重叠的traJ基因的转录，尽管是以不依赖Dam的方式。因此，在肠炎沙门氏菌的Dam(-)宿主中发现的FinP RNA含量降低似乎是由H-NS介导的finP转录抑制所致。
