Mechanosensitive channels in bacterial membranes open or close in response to environmental changes to allow transmembrane transport, including antibiotic uptake and solute efflux. In this paper, we hypothesize that gating of mechanosensitive channels is stimulated by forces through which bacteria adhere to surfaces. Hereto, channel gating is related with adhesion forces to different surfaces of a Staphylococcus aureus strain and its isogenic ΔmscL mutant, deficient in MscL (large) channel gating. Staphylococci becoming fluorescent due to uptake of calcein, increased with adhesion force and were higher in the parent strain (66% when adhering with an adhesion force above 4.0 nN) than in the ΔmscL mutant (40% above 1.2 nN). This suggests that MscL channels open at a higher critical adhesion force than at which physically different, MscS (small) channels open and contribute to transmembrane transport. Uptake of the antibiotic dihydrostreptomycin was monitored by staphylococcal killing. The parent strain exposed to dihydrostreptomycin yielded a CFU reduction of 2.3 log-units when adhering with an adhesion force above 3.5 nN, but CFU reduction remained low (1.0 log-unit) in the mutant, independent of adhesion force. This confirms that large channels open at a higher critical adhesion-force than small channels, as also concluded from calcein transmembrane transport. Collectively, these observations support our hypothesis that adhesion forces to surfaces play an important role, next to other established driving forces, in staphylococcal channel gating. This provides an interesting extension of our understanding of transmembrane antibiotic uptake and solute efflux in infectious staphylococcal biofilms in which bacteria experience adhesion forces from a wide variety of surfaces, like those of other bacteria, tissue cells, or implanted biomaterials.

细菌膜中的机械敏感通道会根据环境变化而打开或关闭，以允许跨膜运输，包括抗生素吸收和溶质外流。在本文中，我们假设机械敏感通道的门控受到细菌粘附到表面的力的刺激。迄今为止，通道门控与金黄色葡萄球菌菌株及其同基因的ΔmscL突变体在MscL（大）通道门控中缺乏的不同表面的粘附力有关。金黄色葡萄球菌由于钙黄绿素的摄取而发荧光，随粘附力的增加而增加，在亲本菌株中（当粘附力高于4.0 nN时，粘附力为66％）高于ΔmscL突变体（高于1.2 nN 40％）。这表明，MscL通道以比物理上不同的MscS（小）通道打开并有助于跨膜运输的临界粘合力更高的临界粘合力打开。通过葡萄球菌杀伤监测抗生素二氢链霉素的摄取。暴露于二氢链霉素的亲本菌株在粘附力高于3.5 nN时粘附时，CFU降低了2.3 log个单位，但突变体中的CFU降低仍然很低（1.0 log单位），与粘附力无关。这也证实了大通道比小通道以更高的临界粘附力打开，这也是钙黄绿素跨膜转运的结论。总而言之，这些观察结果支持了我们的假设，即与表面的附着力仅次于其他既定的驱动力，而起着重要的作用，在葡萄球菌通道门控中。这为我们对感染性葡萄球菌生物膜中跨膜抗生素摄取和溶质外排的理解提供了有趣的扩展，其中细菌会受到多种表面（如其他细菌，组织细胞或植入的生物材料）的粘附力。