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Influence to Biofilm Infection of Surface Protein Mediated by Sortase in Cariogenic Bacteria

分选酶介导的致龋菌表面蛋白生物膜感染的影响

基本信息

批准号：
14571798
负责人：
IGARASHI Takeshi
金额：
$ 1.92万
依托单位：
Showa University
依托单位国家：
日本
项目类别：
Grant-in-Aid for Scientific Research (C)
财政年份：
2002
资助国家：
日本
起止时间：
2002 至 2003
项目状态：
已结题

来源：
https://kaken.nii.ac.jp/en/grant/KAKENHI-PROJECT-14571798/
关键词：
Sortase Streptococcus mutans BIofilm Dextranase Glucan-binding protein C Surface protein antigen LPXTG motif Cell wall anchoring グルカン結合蛋白質 Cell Wall Anchoring Sruface Protein Antigen Glucan Binding Protein デンタルプラーク LPXTG motif

项目摘要

In order to examine influence to biofilm infection of surface protein mediated by the Streptococcus mutans sortase, the sortase gene (srtA) of S.mutans 109c was analyzed and a srtA-deficient mutant of S.mutans 109c was constructed. Surface proteins mediated by the sortase were then identified by western blot analysis and the formation of plaque biofilm by the srtA-deficient mutant of S.mutans 109c. The srtA gene was cloned, the complete nucleotide sequence was determined and then a srtA-deficient mutant of S.mutans 109c was constructed based on the nucleotide sequence. The gene sequence was deposited in the DNA data base of Japan (DDBJ) under the accession number AB089932. Localization change of surface proteins of both wild type 109c and srtA mutant was compared and then the sortase-mediated surface proteins were identified. The result indicated that the sortase mediated the cell-wall anchoring of at least three cariogenic surface proteins: surface protein antigen (PAc), glucan-binding protein (GbpC), dextranase (Dcx). It was also clarified that in the srtA-deficient mutant physiological properties of PAc, GbpC and Dex were lost and the formation of plaque biofilm was inhibited. These results suggested that inactivation of the srtA gene or inhibition of sortase enzyme in S.mutans was useful for the prevention of plaque biofilm formation and subsequent dental caries.

为了研究变形链球菌分选酶介导的表面蛋白对生物膜感染的影响，分析了变形链球菌109 c的分选酶基因（srtA），并构建了srtA缺陷的变形链球菌109 c突变株。然后通过蛋白质印迹分析和变形链球菌109 c的srtA缺陷型突变体的噬菌斑生物膜的形成来鉴定由分选酶介导的表面蛋白。克隆了srtA基因，测定了srtA基因的全序列，构建了变形链球菌109c的srtA缺陷突变株。该基因序列以登录号AB 089932保藏在日本DNA数据库（DDBJ）中。比较野生型109c和srtA突变体表面蛋白的定位变化，鉴定分选酶介导的表面蛋白。结果表明，分选酶介导了至少三种致龋表面蛋白：表面蛋白抗原（PAc）、葡聚糖结合蛋白（GbpC）和葡聚糖酶（Dcx）的细胞壁锚定。还阐明了在srtA缺陷型突变体中，PAc、GbpC和Dex的生理特性丧失，并且菌斑生物膜的形成受到抑制。这些结果表明，srtA基因的失活或分选酶的抑制在变形链球菌中是有用的，以防止菌斑生物膜的形成和随后的龋齿。