Mao Meng-Ying, Yang Ying-Ming, Li Ke-Zeng, Lei Lei, Li Meng, Yang Yan, Tao Xiang, Yin Jia-Xin, Zhang Ru, Ma Xin-Rong, Hu Tao
State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan University Chengdu, China.
State Key Laboratory of Oral Diseases, West China Hospital of Stomatology, Sichuan UniversityChengdu, China; Department of Dentistry, Yan'an Hospital Affiliated to Kunming Medical UniversityKunming, China.
Front Microbiol. 2016 May 10;7:687. doi: 10.3389/fmicb.2016.00687. eCollection 2016.
Dental caries is a biofilm-dependent disease that largely relies on the ability of Streptococcus mutans to synthesize exopolysaccharides. Although the rnc gene is suggested to be involved in virulence mechanisms in many other bacteria, the information regarding it in S. mutans is very limited. Here, using deletion or overexpression mutant assay, we demonstrated that rnc in S. mutans significantly positively regulated exopolysaccharide synthesis and further altered biofilm formation. Meanwhile, the cariogenecity of S. mutans was decreased by deletion of rnc in a specific pathogen-free (SPF) rat model. Interestingly, analyzing the expression at mRNA level, we found the downstream vic locus was repressed by rnc in S. mutans. Using deep sequencing and bioinformatics analysis, for the first time, three putative microRNA-size small RNAs (msRNAs) targeting vicRKX were predicted in S. mutans. The expression levels of these msRNAs were negatively correlated with vicRKX but positively correlated with rnc, indicating rnc probably repressed vicRKX expression through msRNAs at the post-transcriptional level. In all, the results present that rnc has a potential role in the regulation of exopolysaccharide synthesis and can affect vicRKX expressions via post-transcriptional repression in S. mutans. This study provides an alternative avenue for further research aimed at preventing caries.
龋齿是一种依赖生物膜的疾病,很大程度上依赖于变形链球菌合成胞外多糖的能力。尽管rnc基因在许多其他细菌中被认为参与了毒力机制,但在变形链球菌中关于它的信息非常有限。在此,我们通过缺失或过表达突变体分析表明,变形链球菌中的rnc显著正向调节胞外多糖的合成,并进一步改变生物膜的形成。同时,在无特定病原体(SPF)大鼠模型中,通过缺失rnc降低了变形链球菌的致龋性。有趣的是,在mRNA水平分析表达情况时,我们发现变形链球菌中的rnc抑制了下游的vic基因座。通过深度测序和生物信息学分析,首次在变形链球菌中预测到三个靶向vicRKX的假定微小RNA大小的小RNA(msRNA)。这些msRNA的表达水平与vicRKX呈负相关,但与rnc呈正相关,表明rnc可能在转录后水平通过msRNA抑制vicRKX的表达。总之,结果表明rnc在调节胞外多糖合成中具有潜在作用,并且可以通过转录后抑制影响变形链球菌中vicRKX的表达。本研究为进一步预防龋齿的研究提供了一条新途径。