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Infection and Immunity, July 2004, p. 4314-4317, Vol. 72, No. 7
0019-9567/04/$08.00+0 DOI: 10.1128/IAI.72.7.4314-4317.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
Department of Applied Oral Sciences, Faculty of Dentistry,1 Department of Microbiology and Immunology, Faculty of Medicine, Dalhousie University, Halifax, Nova Scotia B3H 3J5,2 Department of Oral Biology, Faculty of Dentistry, University of Manitoba, Winnipeg, Manitoba R3E 0W2, Canada3
Received 26 November 2003/ Returned for modification 9 March 2004/ Accepted 1 April 2004
Streptococcus mutans NG5 failed to anchor antigen P1 to the cell surface, and such a failure could be attributed to a defective SrtA, which was made defective by a point mutation within the srtA gene. Without a functional SrtA, S. mutans NG5 was not able to perform a number of cell surface-related activities, including saliva-mediated adherence and aggregation.
Present address: Sunnybrook and Womens College Health Sciences Centre, University of Toronto, Toronto MN4 3H5, Canada.
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