Harris Leigh K, Theriot Julie A
Biophysics Program, Department of Biochemistry and Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.
Biophysics Program, Department of Biochemistry and Howard Hughes Medical Institute, Stanford University, Stanford, CA 94305, USA.
Cell. 2016 Jun 2;165(6):1479-1492. doi: 10.1016/j.cell.2016.05.045.
Many studies have focused on the mechanisms underlying length and width determination in rod-shaped bacteria. Here, we focus instead on cell surface area to volume ratio (SA/V) and demonstrate that SA/V homeostasis underlies size determination. We propose a model whereby the instantaneous rates of surface and volume synthesis both scale with volume. This model predicts that these relative rates dictate SA/V and that cells approach a new steady-state SA/V exponentially, with a decay constant equal to the volume growth rate. To test this, we exposed diverse bacterial species to sublethal concentrations of a cell wall biosynthesis inhibitor and observed dose-dependent decreases in SA/V. Furthermore, this decrease was exponential and had the expected decay constant. The model also quantitatively describes SA/V alterations induced by other chemical, nutritional, and genetic perturbations. We additionally present evidence for a surface material accumulation threshold underlying division, sensitizing cell length to changes in SA/V requirements.
许多研究都聚焦于杆状细菌长度和宽度确定的潜在机制。在此，我们转而关注细胞表面积与体积比（SA/V），并证明SA/V稳态是大小确定的基础。我们提出一个模型，即表面和体积合成的瞬时速率均与体积成比例。该模型预测，这些相对速率决定SA/V，并且细胞以指数方式趋近新的稳态SA/V，其衰减常数等于体积生长速率。为了验证这一点，我们将多种细菌暴露于亚致死浓度的细胞壁生物合成抑制剂中，观察到SA/V呈剂量依赖性降低。此外，这种降低是指数性的，且具有预期的衰减常数。该模型还定量描述了由其他化学、营养和基因扰动引起的SA/V变化。我们还提供了证据，证明存在一个细胞分裂的表面物质积累阈值，使细胞长度对SA/V需求的变化敏感。
