Section of Preventive and Public Health Dentistry, Division of Oral Health, Growth and Development, Kyushu University Faculty of Dental Science, Fukuoka, Japan.
FEMS Microbiol Lett. 2011 May;318(1):61-7. doi: 10.1111/j.1574-6968.2011.02238.x. Epub 2011 Mar 1.
Streptococcus mutans, a major etiological agent of dental caries, is resistant to bacitracin. Microarray analysis revealed that mbrA and mbrB, encoding a putative ATP-binding cassette transporter, are prominently induced in the presence of bacitracin. On the basis of the latest report that MbrC, a putative response regulator in a two-component signaling system, binds the promoter region of mbrA and thus regulates its transcription, we cut into the mechanism by generating a mutant MbrC (D(54) N-MbrC) that substituted asparagine for aspartate at position 54, the predicted phosphorylation site. MbrC, but not the mutant D(54) N-MbrC, showed affinity for a DNA probe that contained the hypothetical mbrA promoter sequence. Furthermore, we introduced a point mutation (D(54) N-MbrC) into UA159; this mutant strain exhibited neither mbrA induction nor resistance in the presence of bacitracin. These data suggest that the aspartate residue at position 54 of MbrC is a promising candidate for phosphorylation in a bacitracin-sensing system and indispensable for S. mutans bacitracin resistance.
变形链球菌是龋齿的主要病因，对杆菌肽具有耐药性。微阵列分析显示，在杆菌肽存在的情况下，mbrA 和 mbrB（编码一种假定的 ATP 结合盒转运蛋白）明显被诱导。基于最近的一份报告，即双组分信号系统中的假定应答调节子 MbrC 与 mbrA 的启动子区域结合，从而调节其转录，我们通过生成突变体 MbrC（D(54) N-MbrC）来切入该机制，该突变体在 54 位的天冬氨酸被取代为天冬酰胺，这是预测的磷酸化位点。MbrC 而非突变体 D(54) N-MbrC 与包含假定的 mbrA 启动子序列的 DNA 探针具有亲和力。此外，我们在 UA159 中引入了一个点突变（D(54) N-MbrC）；该突变株在杆菌肽存在的情况下既没有诱导 mbrA 也没有表现出杆菌肽耐药性。这些数据表明，MbrC 第 54 位的天冬氨酸残基是杆菌肽感应系统中磷酸化的有前途的候选物，并且对变形链球菌杆菌肽耐药性是不可或缺的。
