Bacterial cell division requires identification of the division site, assembly of the division machinery, and constriction of the cell envelope. These processes are regulated in response to several cellular and environmental signals. Here, we use small molecule iron chelators to characterize the surprising connections between bacterial iron homeostasis and cell division. We demonstrate that iron starvation downregulates the transcription of genes encoding proteins involved in cell division, reduces protein biosynthesis, and prevents correct positioning of the division machinery at the division site. These combined events arrest the constriction of the cell during late stages of cytokinesis in a manner distinct from known mechanisms of inhibiting cell division. Overexpression of genes encoding cell division proteins or iron transporters partially suppresses the biological activity of iron chelators and restores growth and division. We propose a model demonstrating the effect of iron availability on the regulatory mechanisms coordinating division in response to the nutritional state of the cell.

中文翻译：

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小分子螯合剂显示铁饥饿会抑制细菌胞质分裂的晚期

细菌细胞分裂需要确定分裂部位，组装分裂机器和收缩细胞包膜。响应于几种细胞和环境信号来调节这些过程。在这里，我们使用小分子铁螯合剂来表征细菌铁稳态与细胞分裂之间令人惊讶的联系。我们证明，铁饥饿会下调编码参与细胞分裂的蛋白质的基因的转录，减少蛋白质的生物合成，并阻止分裂机构在分裂部位的正确定位。这些组合事件以不同于已知的抑制细胞分裂机制的方式在胞质分裂后期阻止细胞的收缩。编码细胞分裂蛋白或铁转运蛋白的基因的过表达会部分抑制铁螯合剂的生物学活性，并恢复生长和分裂。我们提出了一个模型，该模型展示了铁的有效性对响应细胞营养状态的分裂调控机制的影响。