EzrA, a cell shape regulator contributing to biofilm formation and competitiveness in Streptococcus mutans. (22nd July 2019)

• Record Type: Journal Article
• Authors: Xiang, Zhenting; Li, Zongbo; Ren, Zhi; Zeng, Jumei; Peng, Xian; Li, Yuqing; Li, Jiyao
• Is Part Of: Molecular oral microbiology. Volume 34:Number 5(2019)
• Page Start: 194
• Page End: 208
• Publication Date: 2019-07-22
• Subjects: biofilm formation -- EzrA -- interspecies competition -- Streptococcus mutans; Mouth -- Microbiology -- Periodicals; Respiratory infections -- Microbiology -- Periodicals; Mouth -- Diseases -- Immunological aspects -- Periodicals; 617.522
• DOI: 10.1111/omi.12264
• Languages: English
• ISSNs: 2041-1006

Abstract

Abstract: 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 H2 O2 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. Abstract : Here, the role of EzrA was investigated in Streptococcus mutans 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. Additionally, FtsZ irregularly localized in dividing ezrA mutant cells forming angled division planes. Furthermore, deletion of ezrA resulted in defective biofilm formation and altered biofilm architecture. Unexpectedly, the ezrA mutant exhibited substantially lower tolerance for H2 O2 and reduced competitiveness against Streptococcus sanguinis . Taken together, these results demonstrate that EzrA plays a key role in regulating cell division and biofilm formation in S. mutans .