Cell division is a central process in bacteria and a prerequisite for pathogenicity. Several proteins are involved in this process to ensure the accurate localization and proper function of the division machinery. In Streptococcus mutans, MapZ marks the division sites and position of the Z-ring to regulate cell division; however, whether MapZ deficiency can impair the cariogenic virulence of S. mutans remains unclear. Here, using a phenotypic assay and RNA-seq, we investigated the role of MapZ in cell envelope maintenance, biofilm formation, and stress tolerance in S. mutans. The results show that MapZ is important for normal cell shape and envelope structure, and its deletion causes abnormal septum structure and a thin cell wall. Subsequently, we found that the absence of MapZ leads to a greater level of cell death within 12 h biofilms, but it does not seem to affect biofilm architecture and accumulation. mapZ deletion also results in a decreased acid and osmotic stress tolerance. Furthermore, RNA-seq data reveal that MapZ deficiency causes changes in the expression levels of genes involved in transport systems, sugar metabolism, nature competence, and bacteriocin synthesis. Interestingly, we found that mapZ mutation renders S. mutans more sensitive to chlorhexidine. Taken together, our study suggests that MapZ plays a role in maintaining cell envelope structure and stress tolerance in S. mutans, showing a potential application as a drug target for caries prevention.

中文翻译：

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MapZ缺乏导致包膜结构缺陷并改变变形链球菌的胁迫耐受性

细胞分裂是细菌的核心过程，也是致病性的先决条件。在这个过程中涉及几种蛋白质，以确保分裂机制的准确定位和正常功能。在变形链球菌中，MapZ标记Z环的分裂位点和位置，以调节细胞分裂；然而，MapZ 缺乏是否会损害S. mutans 的致龋毒力仍不清楚。在这里，我们使用表型分析和 RNA-seq，研究了 MapZ 在S. mutans 细胞包膜维持、生物膜形成和胁迫耐受中的作用. 结果表明，MapZ对正常细胞形状和包膜结构很重要，其缺失会导致隔膜结构异常和细胞壁变薄。随后，我们发现 MapZ 的缺失导致 12 小时生物膜内更高水平的细胞死亡，但它似乎不会影响生物膜结构和积累。mapZ缺失还会导致酸和渗透胁迫耐受性降低。此外，RNA-seq 数据表明，MapZ 缺陷会导致涉及转运系统、糖代谢、自然能力和细菌素合成的基因表达水平发生变化。有趣的是，我们发现mapZ突变使S. mutans对氯己定更敏感。总之，我们的研究表明 MapZ 在维持变形链球菌的细胞包膜结构和应激耐受性方面发挥作用，显示出作为预防龋齿的药物靶点的潜在应用。