Bacterial cell division is initiated by tubulin homologue FtsZ that assembles into a ring structure at mid‐cell to facilitate cytokinesis. EzrA has been identified to be implicated in FtsZ‐ring dynamics and cell wall biosynthesis during cell division of Bacillus subtilis and Staphylococcus aureus, the model rod and cocci. However, its role in pathogenic streptococci remains largely unknown. Here, the role of EzrA was investigated in Streptococcus mutans, the primary etiological agent of human dental caries, by constructing an ezrA in‐frame deletion mutant. Our data showed that the ezrA mutant was slow‐growing with a shortened length and extended width round cell shape compared to the wild type, indicating a delay in cell division with abnormalities of peptidoglycan biosynthesis. Additionally, FtsZ irregularly localized in dividing ezrA mutant cells forming angled division planes, potentially contributing to an aberrant cell shape. Furthermore, investigation using single‐species cariogenic biofilm model revealed that deletion of ezrA resulted in defective biofilm formation with less extracellular polysaccharides and altered three‐dimensional biofilm architecture. Unexpectedly, in a dual‐species ecological model, the ezrA mutant exhibited substantially lower tolerance for H₂O₂ and reduced competitiveness against one commensal species, Streptococcus sanguinis. Taken together, these results demonstrate that EzrA plays a key role in regulating cell division and maintaining a normal morphology in S. mutans and is required for its robust biofilm formation/interspecies competition. Therefore, EzrA protein represents a potential therapeutic target in the development of drugs controlling dental caries and other biofilm‐related diseases.

中文翻译：

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EzrA，一种细胞形状调节剂，可促进变形链球菌的生物膜形成和竞争力。

细菌细胞分裂是由微管蛋白同系物FtsZ引发的，该蛋白在细胞中期组装成环结构以促进胞质分裂。EzrA已被证实与枯草芽孢杆菌和金黄色葡萄球菌，模型杆和球菌的细胞分裂过程中的FtsZ环动力学和细胞壁生物合成有关。然而，其在致病性链球菌中的作用仍然未知。在这里，通过构建ezrA框内缺失突变体，研究了EzrA在变形链球菌（人类龋齿的主要病原体）中的作用。我们的数据表明ezrA与野生型相比，该突变体生长缓慢，圆形细胞的长度缩短且宽度扩大，这表明细胞分裂的延迟与肽聚糖生物合成异常有关。另外，FtsZ不规则地位于分裂的ezrA突变细胞中，形成倾斜的分裂平面，可能导致异常的细胞形状。此外，使用单一物种致龋生物膜模型进行的研究表明，ezrA的缺失导致生物膜形成缺陷，细胞外多糖较少，并且三维生物膜结构发生了变化。出乎意料的是，在双物种生态模型中，ezrA突变体表现出对H ₂ O _2的低得多的耐受性并且降低了对一种常见物种血链球菌的竞争能力。综上所述，这些结果表明，EzrA在调节变形链球菌中的细胞分裂和维持正常形态中起关键作用，并且是其强大的生物膜形成/种间竞争所必需的。因此，EzrA蛋白代表了控制龋齿和其他生物膜相关疾病的药物开发中的潜在治疗靶标。