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SMU.940 regulates dextran‐dependent aggregation and biofilm formation in Streptococcus mutans
Author(s) -
Senpuku Hidenobu,
Yonezawa Hideo,
Yoneda Saori,
Suzuki Itaru,
Nagasawa Ryo,
Narisawa Naoki
Publication year - 2018
Publication title -
molecular oral microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.18
H-Index - 77
eISSN - 2041-1014
pISSN - 2041-1006
DOI - 10.1111/omi.12196
Subject(s) - streptococcus mutans , biofilm , dextran , microbiology and biotechnology , chemistry , streptococcus , bacteria , biology , biochemistry , genetics
Summary The oral bacterium Streptococcus mutans is the principal agent in the development of dental caries. Biofilm formation by S. mutans requires bacterial attachment, aggregation, and glucan formation on the tooth surface under sucrose supplementation conditions. Our previous microarray analysis of clinical strains identified 74 genes in S. mutans that were related to biofilm morphology; however, the roles of almost all of these genes in biofilm formation are poorly understood. We investigated the effects of 21 genes randomly selected from our previous study regarding S. mutans biofilm formation, regulation by the complement pathway, and responses to competence‐stimulating peptide. Eight competence‐stimulating peptide‐dependent genes were identified, and their roles in biofilm formation and aggregation were examined by mutational analyses of the S. mutans UA 159 strain. Of these eight genes, the inactivation of the putative hemolysin III family SMU .940 gene of S. mutans UA 159 promoted rapid dextran‐dependent aggregation and biofilm formation in tryptic soy broth without dextrose ( TSB ) with 0.25% glucose and slightly reduced biofilm formation in TSB with 0.25% sucrose. The SMU .940 mutant showed higher expression of GbpC and gbpC gene than wild‐type. GbpC is known to be involved in the dextran‐dependent aggregation of S. mutans . An SMU .940 ‐ gbpC double mutant strain was constructed in the SMU .940 mutant background. The gbpC mutation completely abolished the dextran‐dependent aggregation of the SMU .940 mutant. In addition, the aggregation of the mutant was abrogated by dextranase. These findings suggest that SMU .940 controls GbpC expression, and contributes to the regulation of dextran‐dependent aggregation and biofilm formation.