Fournier B, Hooper D C
Infectious Disease Division and Medical Services, Massachusetts General Hospital, Harvard Medical School, Boston 02114-2696, USA.
J Bacteriol. 2000 Jul;182(14):3955-64. doi: 10.1128/JB.182.14.3955-3964.2000.
A transposition mutant of Staphylococcus aureus was selected from the parent strain MT23142, a derivative of strain 8325. The site of transposition was near the 5' terminus of the gene arlS. ArlS exhibits strong similarities with histidine protein kinases. Sequence analysis suggested that arlS forms an operon with upstream gene arlR. The predicted product of arlR is a member of the OmpR-PhoB family of response regulators. The arlS mutant formed a biofilm on a polystyrene surface unlike the parent strain and the complemented mutant. Biofilm formation was associated with increased primary adherence to polystyrene, whereas cellular adhesion was only slightly decreased. In addition, the arlS mutant exhibited increased autolysis and altered peptidoglycan hydrolase activity compared to the parental strain and to the complemented mutant. As it has been shown for coagulase-negative staphylococci that some autolysins are able to bind polymer surfaces, these data suggest that the two-component regulatory system ArlS-ArlR may control attachment to polymer surfaces by affecting secreted peptidoglycan hydrolase activity. Finally, the arlS mutant showed a dramatic decrease of extracellular proteolytic activity, including serine protease activity, in comparison to the wild-type strain and the complemented mutant, and cells grown in the presence of phenylmethylsulfonyl fluoride (a serine protease inhibitor) showed an increased autolysin activity. Since the locus arlR-arlS strikingly modifies extracellular proteolytic activity, this locus might also be involved in the virulence of S. aureus.
从亲本菌株MT23142（8325菌株的衍生物）中筛选出一株金黄色葡萄球菌转座突变体。转座位点靠近基因arlS的5'末端。ArlS与组氨酸蛋白激酶具有高度相似性。序列分析表明，arlS与上游基因arlR形成一个操纵子。arlR的预测产物是应答调节因子OmpR-PhoB家族的成员。与亲本菌株和互补突变体不同，arlS突变体在聚苯乙烯表面形成了生物膜。生物膜形成与对聚苯乙烯的初始粘附增加有关，而细胞粘附仅略有下降。此外，与亲本菌株和互补突变体相比，arlS突变体表现出更高的自溶活性和改变的肽聚糖水解酶活性。正如凝固酶阴性葡萄球菌所显示的那样，一些自溶素能够结合聚合物表面，这些数据表明双组分调节系统ArlS-ArlR可能通过影响分泌的肽聚糖水解酶活性来控制对聚合物表面的附着。最后，与野生型菌株和互补突变体相比，arlS突变体的细胞外蛋白水解活性，包括丝氨酸蛋白酶活性，显著降低，并且在苯甲基磺酰氟（一种丝氨酸蛋白酶抑制剂）存在下生长的细胞显示出自溶素活性增加。由于arlR-arlS位点显著改变细胞外蛋白水解活性，该位点可能也参与了金黄色葡萄球菌的毒力。
