Genomic and phenotypic characterization of Streptococcus mutans isolates suggests key gene clusters in regulating its interaction with Streptococcus gordonii

Liu, Shanshan; Sun, Yu; Liu, Yudong; Hu, Fuyong; Xu, Liming; Zheng, Qingwei; Wang, Qinglong; Zeng, Guojin; Zhang, Kai

doi:10.3389/fmicb.2022.945108

Cited by 9 publications

(2 citation statements)

References 46 publications

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“…Not only that, we found that the expression of gene cluster smu.137-140 was significantly downregulated. Previous study has shown that this gene cluster is negatively correlated with the activity of S. mutans against S. gordonii (Liu et al, 2022). This seems to be consistent with our finding that in the vicR overexpression strain, this gene cluster is significantly downregulated, and its ability to compete against S. gordonii is enhanced.…”

Section: Discussionsupporting

confidence: 93%

vicR overexpression in Streptococcus mutans causes aggregation and affects interspecies competition

Yan

Gong

et al. 2023

Molecular Oral Microbiology

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Streptococcus mutans is considered to be a major causative agent of dental caries. VicRK is a two‐component signal transduction system (TCSTS) of S. mutans, which can regulate the virulence of S. mutans, such as biofilm formation, exopolysaccharide production, acid production, and acid resistance. Meanwhile, it can also regulate the production of mutacins (nlmC) through the TCSTS ComDE. In this study, we found that the vicR‐overexpressing strain was more likely to aggregate to form cell clusters, leading to the formation of abnormal biofilm; the overexpression of vicR increased the length of the chain of S. mutans. Furthermore, the expression of the mutacins in the vicR overexpression strain was increased under aerobic conditions. Compared with the control strain and the parental strain, the vicR overexpression strain was more competitive against Streptococcus gordonii. But there was no significant difference against Streptococcus sanguinis. In clinical strains, the expression level of vicR was positively correlated with their competitive ability against S. gordonii. Transcriptional profiling revealed 24 significantly upregulated genes in the vicR‐overexpressing strain, including nlmA, nlmB, nlmC, and nlmD encoding mutacins. Electrophoretic mobility shift assays and DNase I footprinting assays confirmed that VicR can directly bind to the promoter sequence of nlmD. Taken together, our findings further demonstrate that VicRK, an important TCSTS of S. mutans, is involved in S. mutans cell morphology and biofilm formation. VicRK regulates the production of more mutacins in S. mutans in response to oxygen stimulation. VicR can bind to the promoter sequence of nlmD, thereby directly regulating the production of mutacins NlmD.

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Section: Discussionsupporting

confidence: 93%

vicR overexpression in Streptococcus mutans causes aggregation and affects interspecies competition

Yan

Gong

et al. 2023

Molecular Oral Microbiology

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“…These 286 isolates were collected from samples of dental plaque obtained from 3-6-year-old children with or without dental caries that are preserved in our laboratory. The isolation and serotype c identification methods for these S. mutans clinical isolates, as well as the activity of these isolates against S. gordonii, were detailed in our prior study [29,30]. All sequences of the 286 S. mutans clinical isolates were submitted to the National Center for Biotechnology Information (NCBI) under the Bio-Project accession number PRJNA1016128.…”

Section: Biological Phenotypementioning

confidence: 99%

SepM mutation in Streptococcus mutans clinical isolates and related function analysis

Liu,

Shao,

Zhang

et al. 2024

BMC Oral Health

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Background Streptococcus mutans (S. mutans) is an important pathogenic bacterium that causes dental caries, while Streptococcus gordonii (S. gordonii) is a non-cariogenic bacterium that inhibits the growth of S. mutans. The SepM protein can promote the inhibitory ability of S. mutans against S. gordonii by cleaving CSP-21 and activating the ComDE two-component system. This study was designed to explore sepM mutation in S. mutans clinical isolates and related function in the regulation of interactions with S. gordonii. Methods The S. mutans clinical strains that can inhibit the growth of S. gordonii constitute the inhibitory group. 286 C-serotype S. mutans strains were categorized into S. gordonii inhibitory (n = 114) and non-inhibitory bacteria (n = 172). We detected sanger sequencing of sepM gene, the expression levels of related genes and proteins in clinical isolates, obtained prokaryotic expression and purification of mutated proteins, and analyzed the effect of the target mutations on the binding between SepM and CSP-21. Results We found that C482T, G533A, and G661A missense mutations were presented at significantly higher frequency in the inhibitory group relative to the non-inhibitory group. There was no significant difference in the expression of the sepM gene between selected clinical isolates harboring the G533A mutation and the control group. The expression levels of SepM, phosphorylated ComD, and ComE in the mutation group were significantly higher than those in the control group. SepM_control and SepM_D221N (G661A at the gene level) were found to contain two residues close to the active center while SepM_G178D (G533A at the gene level) contained three residues close to the active center. At 25 °C and a pH of 5.5, SepM_D221N (G661A) exhibited higher affinity for CSP-21 (KD = 8.25 µM) than did the SepM control (KD = 33.1 µM), and at 25 °C and a pH of 7.5, SepM_G178D (G533A) exhibited higher affinity (KD = 3.02 µM) than the SepM control (KD = 15.9 µM). It means that it is pH dependent. Conclusions Our data suggest that increased cleavage of CSP-21 by the the mutant SepM may be a reason for the higher inhibitory effect of S. mutans on S. gordonii .

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An Introduction to the Human Microbiome

Kotthapalli,

Archer

2024

Human Microbiome

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Genomic and phenotypic characterization of Streptococcus mutans isolates suggests key gene clusters in regulating its interaction with Streptococcus gordonii

Cited by 9 publications

References 46 publications

vicR overexpression in Streptococcus mutans causes aggregation and affects interspecies competition

vicR overexpression in Streptococcus mutans causes aggregation and affects interspecies competition

SepM mutation in Streptococcus mutans clinical isolates and related function analysis

An Introduction to the Human Microbiome

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