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MapZ 缺乏导致变形链球菌包膜结构缺陷和应激耐受性改变。

MapZ deficiency leads to defects in the envelope structure and changes stress tolerance of Streptococcus mutans.

机构信息

Department of Geriatric Dentistry, Peking University Hospital of Stomatology, Beijing, P. R. China.

National Engineering Laboratory for Digital and Material Technology of Stomatology, NMPA Key Laboratory for Dental Materials, Beijing Laboratory of Biomedical Materials, Peking University Hospital of Stomatology, Beijing, P. R. China.

出版信息

Mol Oral Microbiol. 2021 Dec;36(6):295-307. doi: 10.1111/omi.12352. Epub 2021 Sep 16.

Abstract

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.

摘要

细胞分裂是细菌的核心过程,也是致病性的前提。有几种蛋白质参与这个过程,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 标记了分裂位点和 Z 环的位置,以调节细胞分裂;然而,MapZ 缺乏是否会损害变形链球菌的致龋毒力尚不清楚。在这里,我们使用表型测定和 RNA-seq 研究了 MapZ 在变形链球菌的细胞包膜维持、生物膜形成和应激耐受中的作用。结果表明,MapZ 对于正常的细胞形状和包膜结构很重要,其缺失导致异常的隔膜结构和细胞壁变薄。随后,我们发现 MapZ 的缺失导致 12 小时生物膜内细胞死亡水平增加,但似乎不影响生物膜结构和积累。mapZ 缺失也导致酸和渗透压应激耐受性降低。此外,RNA-seq 数据显示,MapZ 缺乏导致参与运输系统、糖代谢、自然感受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 突变使变形链球菌对洗必泰更敏感。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中发挥作用,显示出作为预防龋齿的药物靶点的潜力。

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