Department of Microbiology and Immunology, College of Physicians and Surgeons, Columbia University, New York, NY 10032, USA.
Mol Microbiol. 2010 May;76(4):956-70. doi: 10.1111/j.1365-2958.2010.07155.x. Epub 2010 Apr 1.
During Bacillus subtilis sporulation, an endocytic-like process called engulfment results in one cell being entirely encased in the cytoplasm of another cell. The driving force underlying this process of membrane movement has remained unclear, although components of the machinery have been characterized. Here we provide evidence that synthesis of peptidoglycan, the rigid, strength bearing extracellular polymer of bacteria, is a key part of the missing force-generating mechanism for engulfment. We observed that sites of peptidoglycan synthesis initially coincide with the engulfing membrane and later with the site of engulfment membrane fission. Furthermore, compounds that block muropeptide synthesis or polymerization prevented membrane migration in cells lacking a component of the engulfment machinery (SpoIIQ), and blocked the membrane fission event at the completion of engulfment in all cells. In addition, these compounds inhibited bulge and vesicle formation that occur in spoIID mutant cells unable to initiate engulfment, as did genetic ablation of a protein that polymerizes muropeptides. This is the first report to our knowledge that peptidoglycan synthesis is necessary for membrane movements in bacterial cells and has implications for the mechanism of force generation during cytokinesis.
在枯草芽孢杆菌孢子形成过程中,一种称为吞噬的内吞样过程导致一个细胞完全被另一个细胞的细胞质包裹。虽然已经鉴定了该机制的组件,但该过程中膜运动的驱动力仍不清楚。在这里,我们提供的证据表明,肽聚糖的合成,即细菌的刚性、承载强度的细胞外聚合物,是吞噬作用缺失力产生机制的关键部分。我们观察到肽聚糖合成的部位最初与吞噬膜重合,随后与吞噬膜分裂的部位重合。此外,阻断肽聚糖合成或聚合的化合物可防止在缺乏吞噬机制组件(SpoIIQ)的细胞中膜迁移,并阻止所有细胞中吞噬作用完成时的膜分裂事件。此外,这些化合物抑制了在无法开始吞噬的 spoIID 突变细胞中发生的隆起和囊泡形成,就像聚合肽聚糖的蛋白质的遗传缺失一样。这是我们所知的第一个报道,即肽聚糖合成对于细菌细胞中膜运动是必需的,并且对细胞分裂过程中力产生的机制有影响。