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Antimicrobial Agents and Chemotherapy, December 2002, p. 3756-3764, Vol. 46, No. 12
0066-4804/02/$04.00+0     DOI: 10.1128/AAC.46.12.3756-3764.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.

Genes Involved in Bacitracin Resistance in Streptococcus mutans{dagger}

Hiromasa Tsuda,1 Yoshihisa Yamashita,2* Yukie Shibata,1 Yoshio Nakano,1 and Toshihiko Koga1,{ddagger}

Department of Preventive Dentistry, Kyushu University Faculty of Dental Science, Fukuoka 812-8582,1 Department of Oral Health Sciences, Nihon University School of Dentistry, Tokyo 101-8310, Japan2

Received 28 January 2002/ Returned for modification 8 April 2002/ Accepted 16 August 2002

Streptococcus mutans is resistant to bacitracin, which is a peptide antibiotic produced by certain species of Bacillus. The purpose of this study was to clarify the bacitracin resistance mechanism of S. mutans. We cloned and sequenced two S. mutans loci that are involved in bacitracin resistance. The rgp locus, which is located downstream from rmlD, contains six rgp genes (rgpA to rgpF) that are involved in rhamnose-glucose polysaccharide (RGP) synthesis in S. mutans. The inactivation of RGP synthesis in S. mutans resulted in an approximately fivefold-higher sensitivity to bacitracin relative to that observed for the wild-type strain Xc. The second bacitracin resistance locus comprised four mbr genes (mbrA, mbrB, mbrC, and mbrD) and was located immediately downstream from gtfC, which encodes the water-insoluble glucan-synthesizing enzyme. Although the bacitracin sensitivities of mutants that had defects in flanking genes were similar to that of the parental strain Xc, mutants that were defective in mbrA, mbrB, mbrC, or mbrD were about 100 to 120 times more sensitive to bacitracin than strain Xc. In addition, a mutant that was defective in all of the mbrABCD genes and rgpA was more sensitive to bacitracin than either the RGP or Mbr mutants. We conclude that RGP synthesis is related to bacitracin resistance in S. mutans and that the mbr genes modulate resistance to bacitracin via an unknown mechanism that is independent of RGP synthesis.

* Corresponding author. Mailing address: Department of Oral Health Sciences, Nihon University School of Dentistry, 1-8-13 Kandasurugadai, Chiyoda-ku, Tokyo 101-8310, Japan. Phone: 81-3-3219-8118. Fax: 81-3-3219-8138. E-mail: yamashita{at}dent.nihon-u.ac.jp.

{dagger} Dedicated to the memory of Toshihiko Koga, esteemed researcher and our mentor.

{ddagger} Deceased.

Antimicrobial Agents and Chemotherapy, December 2002, p. 3756-3764, Vol. 46, No. 12
0066-4804/02/$04.00+0     DOI: 10.1128/AAC.46.12.3756-3764.2002
Copyright © 2002, American Society for Microbiology. All Rights Reserved.



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