In all living organisms, genome replication and cell division must be coordinated to produce viable offspring. In the event of DNA damage, bacterial cells employ the SOS response to simultaneously express damage repair systems and halt cell division. Extensive characterization of SOS-controlled cell division inhibition in Escherichia coli has laid the ground for a long-standing paradigm where the cytosolic SulA protein inhibits polymerization of the central division protein, FtsZ, and thereby prevents recruitment of the division machinery at the future division site. Within the last decade, it has become clear that another, likely more general, paradigm exists, at least within the broad group of Gram-positive bacterial species, namely membrane-localized, SOS-induced cell division inhibition. We recently identified such an inhibitor in Staphylococci, SosA, and established a model for SosA-mediated cell division inhibition in Staphylococcus aureus in response to DNA damage. SosA arrests cell division subsequent to the septal localization of FtsZ and later membrane-bound division proteins, while preventing progression to septum closure, leading to synchronization of cells at this particular stage. A membrane-associated protease, CtpA negatively regulates SosA activity and likely allows growth to resume once conditions are favorable. Here, we provide a brief summary of our findings in the context of what already is known for other membrane cell division inhibitors and we emphasize how poorly characterized these intriguing processes are mechanistically. Furthermore, we put some perspective on the relevance of our findings and future developments within the field.

中文翻译：

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葡萄球菌中的SosA：是细菌中膜定位，SOS诱导的细胞分裂抑制的范例的补充。

在所有活生物体中，必须协调基因组复制和细胞分裂，以产生有活力的后代。在DNA受损的情况下，细菌细胞利用SOS响应同时表达损害修复系统和停止细胞分裂。大肠杆菌中SOS控制的细胞分裂抑制的广泛表征为长期存在的范例奠定了基础，在该范例中，胞质SulA蛋白抑制了中央分裂蛋白FtsZ的聚合，从而阻止了未来分裂部位募集分裂机制。在过去的十年中，已经清楚的是，至少在广泛的革兰氏阳性细菌种类中存在着另一个可能更普遍的范式，即膜定位的SOS诱导的细胞分裂抑制。我们最近在葡萄球菌，SosA中确定了这种抑制剂，并建立了响应DNA损伤的金黄色葡萄球菌中SosA介导的细胞分裂抑制的模型。SosA在FtsZ的间隔定位和随后的膜结合分裂蛋白之后阻止细胞分裂，同时防止进展为间隔闭合，从而导致该特定阶段的细胞同步。膜相关蛋白酶CtpA负调节SosA活性，一旦条件有利，可能使生长恢复。在这里，我们将在其他膜细胞分裂抑制剂的已知背景下简要概述我们的发现，并且我们强调这些有趣的过程在机理上的描述性很差。此外，