To maximize their fitness, cells must be able to respond effectively to stresses. This demands making trade-offs between processes that conserve resources to promote survival, and processes that use resources to promote growth and division. Understanding the nature of these trade-offs and the physics underlying them remains an outstanding challenge. Here we combine single-cell experiments and theoretical modelling to propose a mechanism for antibiotic adaptation through mechanical feedback between cell growth and morphology. Under long-term exposure to sublethal doses of ribosome-targeting antibiotics, we find that Caulobacter crescentus cells can recover their pre-stimulus growth rates and undergo dramatic changes in cell shape. Upon antibiotic removal, cells recover their original forms over multiple generations. These phenomena are explained by a physical theory of bacterial growth, which demonstrates that an increase in cell width and curvature promotes faster growth under protein synthesis inhibition. Shape changes thereby make bacteria more adaptive to surviving antibiotics.

为了最大限度地提高它们的适应性，细胞必须能够有效地应对压力。这需要在节约资源以促进生存的过程与使用资源促进增长和分裂的过程之间进行权衡。了解这些权衡的性质及其背后的物理原理仍然是一项艰巨的挑战。在这里，我们结合单细胞实验和理论建模，通过细胞生长和形态之间的机械反馈提出抗生素适应机制。在长期暴露于亚致死剂量的核糖体靶向抗生素下，我们发现新月形茎杆菌细胞可以恢复其刺激前的生长速率并经历细胞形状的巨大变化。去除抗生素后，细胞会在多代后恢复其原始形式。这些现象可以用细菌生长的物理理论来解释，这表明细胞宽度和曲率的增加在蛋白质合成抑制下促进了更快的生长。形状的变化从而使细菌更适应幸存的抗生素。