The cariogenic pathogen Streptococcus mutans effectively utilizes dietary sucrose for the synthesis of exopolysaccharides (EPS), which act as a scaffold for its biofilm and thus contribute to its cariogenic pathogenicity. Dextranase (Dex), which is a type of glucanase, participates in the degradation of water‐soluble glucan (WSG); however, the structural features of the EPS regulated by the dexAgene have received limited attention. Our recent studies reported novel protocols to fractionate and analyzed the structural characteristics of glucans from S mutans biofilms. In this study, we identify the role of the S mutans dexAgene in dextran‐dependent aggregation in biofilm formation. Our results show that deletion of dexA (SmudexA) results in increased transcription of EPS synthesis‐related genes, including gtfB, gtfD, and ftf. Interestingly, we reveal that inactivating the dexA gene may lead to elevated WSG synthesis in S mutans , which results in dysregulated cariogenicity in vivo. Furthermore, structural analysis provides new insights regarding the lack of mannose monosaccharides, especially in the WSG synthesis of the SmudexA mutants. The biofilm phenotypes that are associated with the reduced glucose monosaccharide composition in both WSG and water‐insoluble glucan shift the dental biofilm to reduce the cariogenic incidence of the SmudexA mutants. Taken together, these data reveal that EPS synthesis fine‐tuning by the dexA gene results in a densely packed EPS matrix that may impede the glucose metabolism of WSG, thereby leading to the lack of an energy source for the bacteria. These results highlight dexA targeting as a potentially effective tool in dental caries management.

中文翻译：

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变形链球菌dexA基因调控的水溶性葡聚糖合成影响生物膜聚集和致癌性。

致癌病原体变形链球菌有效利用膳食蔗糖合成胞外多糖（EPS），胞外多糖充当其生物膜的支架，因此有助于其致癌性。葡聚糖酶的一种是葡聚糖酶（Dex），它参与水溶性葡聚糖（WSG）的降解。然而，由dexA基因调控的EPS的结构特征受到了有限的关注。我们最近的研究报告了新颖的协议，以分离和分析变形链球菌生物膜中的葡聚糖的结构特征。在这项研究中，我们确定了变形链球菌dexA基因在生物膜形成中依赖于葡聚糖的聚集中的作用。我们的结果表明dexA的缺失（SmudexA）导致EPS合成相关基因（包括gtfB，g tfD和ftf）的转录增加。有趣的是，我们揭示了灭活dexA基因可能导致变形链球菌中WSG合成增加，从而导致体内致龋性失调。此外，结构分析提供了有关缺少甘露糖单糖的新见解，尤其是在SmudexA突变体的WSG合成中。与WSG和水不溶性葡聚糖中葡萄糖单糖成分减少相关的生物膜表型改变了牙齿生物膜，从而降低了SmudexA的龋齿发生率突变体。综上所述，这些数据表明，通过dexA基因进行的EPS合成微调导致EPS基质密集，这可能会阻碍WSG的葡萄糖代谢，从而导致细菌缺乏能源。这些结果突出了dexA靶向在龋齿管理中的潜在有效工具。