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Applied and Environmental Microbiology, November 2009, p. 7037-7043, Vol. 75, No. 22
0099-2240/09/$08.00+0     doi:10.1128/AEM.01015-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Role of the Streptococcus mutans irvA Gene in GbpC-Independent, Dextran-Dependent Aggregation and Biofilm Formation{triangledown}

Min Zhu,1 Dragana Ajdic,2 Yuan Liu,1 David Lynch,1 Justin Merritt,2 and Jeffrey A. Banas1*

Dows Institute for Dental Research, Department of Pediatric Dentistry, College of Dentistry, University of Iowa, Iowa City, Iowa 52242,1 University of Oklahoma Health Sciences Center, Oklahoma City, Oklahoma 731042

Received 4 May 2009/ Accepted 21 September 2009

Dextran-dependent aggregation (DDAG) of Streptococcus mutans is an in vitro phenomenon that is believed to represent a property of the organism that is beneficial for sucrose-dependent biofilm development. GbpC, a cell surface glucan-binding protein, is responsible for DDAG in S. mutans when cultured under defined stressful conditions. Recent reports have described a putative transcriptional regulator gene, irvA, located just upstream of gbpC, that is normally repressed by the product of an adjacent gene, irvR. When repression of irvA is relieved, there is a resulting increase in the expression of GbpC and decreases in competence and synthesis of the antibiotic mutacin I. This study examined the role of irvA in DDAG and biofilm formation by engineering strains that overexpressed irvA (IrvA+) on an extrachromosomal plasmid. The IrvA+ strain displayed large aggregation particles that did not require stressful growth conditions. A novel finding was that overexpression of irvA in a gbpC mutant background retained a measure of DDAG, albeit very small aggregation particles. Biofilms formed by the IrvA+ strain in the parental background possessed larger-than-normal microcolonies. In a gbpC mutant background, the overexpression of irvA reversed the fragile biofilm phenotype normally associated with loss of GbpC. Real-time PCR and Northern blot analyses found that expression of gbpC did not change significantly in the IrvA+ strain but expression of spaP, encoding the major surface adhesin P1, increased significantly. Inactivation of spaP eliminated the small-particle DDAG. The results suggest that IrvA promotes DDAG not only by GbpC, but also via an increase in P1.

* Corresponding author. Mailing address: Dows Institute for Dental Research, University of Iowa, N436 Dental Science Building, Iowa City, IA 52242. Phone: (319) 335-9911. Fax: (319) 335-8895. E-mail: Jeffrey-Banas{at}uiowa.edu

{triangledown} Published ahead of print on 25 September 2009.

Applied and Environmental Microbiology, November 2009, p. 7037-7043, Vol. 75, No. 22
0099-2240/09/$08.00+0     doi:10.1128/AEM.01015-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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