Balbontín Roberto, Rowley Gary, Pucciarelli M Graciela, López-Garrido Javier, Wormstone Yvette, Lucchini Sacha, García-Del Portillo Francisco, Hinton Jay C D, Casadesús Josep
Departamento de Genética, Facultad de Biología, Universidad de Sevilla, 41080 Seville, Spain.
J Bacteriol. 2006 Dec;188(23):8160-8. doi: 10.1128/JB.00847-06. Epub 2006 Sep 22.
Transcriptomic analyses during growth in Luria-Bertani medium were performed in strain SL1344 of Salmonella enterica serovar Typhimurium and in two isogenic derivatives lacking Dam methylase. More genes were repressed than were activated by Dam methylation (139 versus 37). Key genes that were differentially regulated by Dam methylation were verified independently. The largest classes of Dam-repressed genes included genes belonging to the SOS regulon, as previously described in Escherichia coli, and genes of the SOS-inducible Salmonella prophages ST64B, Gifsy-1, and Fels-2. Dam-dependent virulence-related genes were also identified. Invasion genes in pathogenicity island SPI-1 were activated by Dam methylation, while the fimbrial operon std was repressed by Dam methylation. Certain flagellar genes were repressed by Dam methylation, and Dam(-) mutants of S. enterica showed reduced motility. Altered expression patterns in the absence of Dam methylation were also found for the chemotaxis genes cheR (repressed by Dam) and STM3216 (activated by Dam) and for the Braun lipoprotein gene, lppB (activated by Dam). The requirement for DNA adenine methylation in the regulation of specific virulence genes suggests that certain defects of Salmonella Dam(-) mutants in the mouse model may be caused by altered patterns of gene expression.
在鼠伤寒沙门氏菌血清型鼠伤寒杆菌的SL1344菌株以及两个缺乏Dam甲基化酶的同基因衍生物中,对其在Luria-Bertani培养基中生长期间进行了转录组分析。受Dam甲基化抑制的基因比被激活的基因更多(139个对37个)。通过Dam甲基化差异调节的关键基因进行了独立验证。受Dam抑制的最大类基因包括属于SOS调节子的基因,如先前在大肠杆菌中所描述的,以及SOS诱导性沙门氏菌原噬菌体ST64B、Gifsy-1和Fels-2的基因。还鉴定出了与Dam依赖性毒力相关的基因。致病岛SPI-1中的侵袭基因通过Dam甲基化被激活,而菌毛操纵子std则被Dam甲基化抑制。某些鞭毛基因被Dam甲基化抑制,肠炎沙门氏菌的Dam(-)突变体显示出运动性降低。在缺乏Dam甲基化的情况下,趋化基因cheR(被Dam抑制)和STM3216(被Dam激活)以及布劳恩脂蛋白基因lppB(被Dam激活)的表达模式也发生了改变。特定毒力基因调控中对DNA腺嘌呤甲基化的需求表明,沙门氏菌Dam(-)突变体在小鼠模型中的某些缺陷可能是由基因表达模式的改变引起的。