Sun Yuting, Chen Hong, Xu Mengmeng, He Liwen, Mao Hongchen, Yang Shiyao, Qiao Xin, Yang Deqin
Department of Endodontics, Stomatological Hospital of Chongqing Medical University, Chongqing, China.
Chongqing Key Laboratory of Oral Diseases and Biomedical Sciences, Chongqing, China.
J Oral Microbiol. 2023 Apr 28;15(1):2204250. doi: 10.1080/20002297.2023.2204250. eCollection 2023.
( ) is a pivotal cariogenic pathogen contributing to its multiple virulence factors, one of which is synthesizing exopolysaccharides (EPS). VicK, a sensor histidine kinase, plays a major role in regulating genes associated with EPS synthesis and adhesion. Here we first identified an antisense RNA (AS) bound with into double-stranded RNA (dsRNA).
This study aims to investigate the effect and mechanism of AS in the EPS metabolism and cariogenesis of .
The phenotypes of biofilm were detected by scanning electron microscopy (SEM), gas chromatography-mass spectrometery (GC-MS) , gel permeation chromatography (GPC) , transcriptome analysis and Western blot. Co-immunoprecipitation (Co-ip) assay and enzyme activity experiment were adopted to investigate the mechanism of AS regulation. Caries animal models were developed to study the relationship between AS and cariogenicity of
Overexpression of AS can inhibit the growth of biofilm, reduce the production of EPS and alter genes and protein related to EPS metabolism. AS can adsorb RNase III to regulate and affect the cariogenicity of .
AS regulates at the transcriptional and post-transcriptional levels, effectively inhibits EPS synthesis and biofilm formation and reduces its cariogenicity .
（ ）是一种关键的致龋病原体，其多种毒力因子之一是合成胞外多糖（EPS）。VicK是一种传感组氨酸激酶，在调节与EPS合成和黏附相关的基因中起主要作用。在此，我们首次鉴定出一种与（ ）结合形成双链RNA（dsRNA）的反义RNA（AS）。
本研究旨在探讨AS在（ ）的EPS代谢和致龋过程中的作用及机制。
通过扫描电子显微镜（SEM）、气相色谱 - 质谱联用（GC - MS）、凝胶渗透色谱（GPC）、转录组分析和蛋白质印迹法检测生物膜的表型。采用免疫共沉淀（Co - ip）试验和酶活性实验研究AS的调控机制。建立龋齿动物模型以研究AS与（ ）致龋性之间的关系。
AS的过表达可抑制生物膜生长，减少EPS产生，并改变与EPS代谢相关的基因和蛋白质。AS可吸附核糖核酸酶III来调节（ ）并影响其致龋性。
AS在转录和转录后水平调节（ ），有效抑制EPS合成和生物膜形成，并降低其致龋性。
