Liu George S, Bratton Benjamin P, Gitai Zemer, Shaevitz Joshua W
Department of Physics, Princeton University, Princeton, NJ, United States of America.
Lewis-Sigler Institute for Integrative Genomics, Princeton University, Princeton, NJ, United States of America.
PLoS One. 2017 Oct 4;12(10):e0185810. doi: 10.1371/journal.pone.0185810. eCollection 2017.
Accumulating evidence suggests that molecular motors contribute to the apparent diffusion of molecules in cells. However, current literature lacks evidence for an active process that drives diffusive-like motion in the bacterial membrane. One possible mechanism is cell wall synthesis, which involves the movement of protein complexes in the cell membrane circumferentially around the cell envelope and may generate currents in the lipid bilayer that advectively transport other transmembrane proteins. We test this hypothesis in Escherichia coli using drug treatments that slow cell wall synthesis and measure their effect on the diffusion of the transmembrane protein mannitol permease using fluorescence recovery after photobleaching. We found no clear decrease in diffusion in response to vancomycin and no decrease in response to mecillinam treatment. These results suggest that cell wall synthesis is not an active contributor to mobility in the cytoplasmic membrane.
越来越多的证据表明，分子马达有助于细胞内分子的表观扩散。然而，目前的文献缺乏驱动细菌膜中类似扩散运动的主动过程的证据。一种可能的机制是细胞壁合成，这涉及细胞膜中蛋白质复合物围绕细胞包膜的圆周运动，并可能在脂质双层中产生电流，从而平流运输其他跨膜蛋白。我们在大肠杆菌中使用减缓细胞壁合成的药物处理来检验这一假设，并通过光漂白后的荧光恢复来测量它们对跨膜蛋白甘露醇通透酶扩散的影响。我们发现，对万古霉素的反应中扩散没有明显下降，对美西林治疗也没有下降。这些结果表明，细胞壁合成不是细胞质膜流动性的主动贡献因素。
