Mutation of the Streptococcus gordonii Thiol-Disulfide Oxidoreductase SdbA Leads to Enhanced Biofilm Formation Mediated by the CiaRH Two-Component Signaling System

被引:10
作者
Davey, Lauren [1 ,2 ,3 ]
Halperin, Scott A. [1 ,2 ,3 ,4 ]
Lee, Song F. [1 ,2 ,3 ,4 ,5 ]
机构
[1] Dalhousie Univ, Dept Microbiol & Immunol, Halifax, NS B3H 1X5, Canada
[2] Dalhousie Univ, Canadian Ctr Vaccinol, Halifax, NS B3K 6R8, Canada
[3] IWK Hlth Ctr, Halifax, NS B3K 6R8, Canada
[4] Dalhousie Univ, Dept Pediat, Fac Med, Halifax, NS B3K 6R8, Canada
[5] Dalhousie Univ, Dept Appl Oral Sci, Fac Med, Halifax, NS B3H 4R2, Canada
基金
加拿大自然科学与工程研究理事会;
关键词
BINDING-PROTEIN-B; REGULATORY SYSTEM; RESPONSE REGULATOR; ORAL COLONIZATION; IMMUNE-RESPONSES; STRESS TOLERANCE; PNEUMONIAE R6; A ABPA; COMPETENCE; MUTANS;
D O I
10.1371/journal.pone.0166656
中图分类号
O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];
学科分类号
07 ; 0710 ; 09 ;
摘要
Streptococcus gordonii is a commensal inhabitant of human oral biofilms. Previously, we identified an enzyme called SdbA that played an important role in biofilm formation by S. gordonii. SdbA is thiol-disulfide oxidoreductase that catalyzes disulfide bonds in secreted proteins. Surprisingly, inactivation of SdbA results in enhanced biofilm formation. In this study we investigated the basis for biofilm formation by the Delta sdbA mutant. The results revealed that biofilm formation was mediated by the interaction between the CiaRH and ComDE twocomponent signalling systems. Although it did not affect biofilm formation by the S. gordonii parent strain, CiaRH was upregulated in the Delta sdbA mutant and it was essential for the enhanced biofilm phenotype. The biofilm phenotype was reversed by inactivation of CiaRH or by the addition of competence stimulating peptide, the production of which is blocked by CiaRH activity. Competition assays showed that the enhanced biofilm phenotype also corresponded to increased oral colonization in mice. Thus, the interaction between SdbA, CiaRH and ComDE affects biofilm formation both in vitro and in vivo.
引用
收藏
页数:18
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