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Journal of Bacteriology, April 2007, p. 3166-3175, Vol. 189, No. 8
0021-9193/07/$08.00+0     doi:10.1128/JB.01808-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

Genome of the Opportunistic Pathogen Streptococcus sanguinis{triangledown} ,{dagger}

Ping Xu,1,2,3,{ddagger} Joao M. Alves,2,3,{ddagger} Todd Kitten,1,2,3 Arunsri Brown,1,§ Zhenming Chen,2,3,¶ Luiz S. Ozaki,2,3 Patricio Manque,2,3 Xiuchun Ge,1 Myrna G. Serrano,2,3 Daniela Puiu,2,|| Stephanie Hendricks,3 Yingping Wang,2,3 Michael D. Chaplin,2 Doruk Akan,2,{dagger}{dagger} Sehmi Paik,1,3,{ddagger}{ddagger} Darrell L. Peterson,4 Francis L. Macrina,1,2,3* and Gregory A. Buck2,3*

Philips Institute of Oral and Craniofacial Molecular Biology, Virginia Commonwealth University, Richmond, Virginia 23298-0566,1 Center for the Study of Biological Complexity, Virginia Commonwealth University, Richmond, Virginia 23284-2030,2 Department of Microbiology and Immunology, Virginia Commonwealth University, Richmond, Virginia 23298-0678,3 Department of Biochemistry and Molecular Biophysics, Virginia Commonwealth University, Richmond, Virginia 23298-06144

Received 30 November 2006/ Accepted 29 January 2007

The genome of Streptococcus sanguinis is a circular DNA molecule consisting of 2,388,435 bp and is 177 to 590 kb larger than the other 21 streptococcal genomes that have been sequenced. The G+C content of the S. sanguinis genome is 43.4%, which is considerably higher than the G+C contents of other streptococci. The genome encodes 2,274 predicted proteins, 61 tRNAs, and four rRNA operons. A 70-kb region encoding pathways for vitamin B12 biosynthesis and degradation of ethanolamine and propanediol was apparently acquired by horizontal gene transfer. The gene complement suggests new hypotheses for the pathogenesis and virulence of S. sanguinis and differs from the gene complements of other pathogenic and nonpathogenic streptococci. In particular, S. sanguinis possesses a remarkable abundance of putative surface proteins, which may permit it to be a primary colonizer of the oral cavity and agent of streptococcal endocarditis and infection in neutropenic patients.

* Corresponding author. Mailing address: Center for the Study of Biological Complexity, Virginia Commonwealth University, Richmond, VA 23284-2030. Phone for Francis L. Macrina: (804) 827-2622. Fax: (804) 828-2051. E-mail: macrina{at}vcu.edu. Phone for Gregory A. Buck: (804) 828-2318. Fax: (804) 828-1397. E-mail: gabuck{at}vcu.edu

{triangledown} Published ahead of print on 2 February 2007.

{dagger} Supplemental material for this article may be found at http://jb.asm.org/.

{ddagger} P.X. and J.M.A. contributed equally to this work.

§ Present address: Office of International Extramural Activities, Division of Extramural Activities, NIH/NIAID, Room 2155, Bethesda, MD 20892-7610.

Present address: College of Biological & Environmental Engineering, Zhejiang University of Technology, 18 ChaoWang Road, Hangzhou, Zhejiang 310032, China.

|| Present address: The Institute for Genome Research, 9712 Medical Center Drive, Rockville, MD 20850.

{dagger}{dagger} Present address: Department of Systems and Information Engineering, University of Virginia, P.O. Box 400747, 151 Engineer's Way, Charlottesville, VA 22904.

{ddagger}{ddagger} Present address: Department of Biomedical Sciences, University of Maryland Dental School, 650 W. Baltimore Street, Baltimore, MD 21201.

Journal of Bacteriology, April 2007, p. 3166-3175, Vol. 189, No. 8
0021-9193/07/$08.00+0     doi:10.1128/JB.01808-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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