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Journal of Bacteriology, June 2009, p. 3588-3593, Vol. 191, No. 11
0021-9193/09/$08.00+0     doi:10.1128/JB.00142-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Diversifying and Stabilizing Selection of Sialidase and N-Acetylneuraminate Catabolism in Mycoplasma synoviae{triangledown} ,§

Meghan May and Daniel R. Brown*

Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, Florida 32611-0880

Received 2 February 2009/ Accepted 24 March 2009

Sialidase activity varies widely among strains and tends to correlate with strain virulence in the avian pathogen Mycoplasma synoviae. To characterize the forms of selection acting on enzymes required for sialic acid scavenging and catabolism, the ratios of nonsynonymous (Ka) to synonymous (Ks) mutation frequency were calculated for codons in the sialidase gene of 16 strains of M. synoviae and for its nearly identical homolog in four strains of Mycoplasma gallisepticum. The Ka/Ks ({omega}) values for the linked genes required for nutritive N-acetylneuraminate catabolism (nanA, nagC, nanE, nagA, and nagB) from nine strains of M. synoviae were also determined. To provide context, {omega} was determined for all corresponding genes of 26 strains of Clostridium perfringens and Streptococcus pneumoniae. Bayesian models of sequence evolution showed that only the sialidase of M. synoviae was under significant (P < 0.001) diversifying selection, while the M. synoviae genes for N-acetylneuraminate catabolism and all genes examined from M. gallisepticum, C. perfringens, and S. pneumoniae were under neutral to stabilizing selection. Diversifying selection acting on the sialidase of M. synoviae, but not on the sialidase of M. gallisepticum or the sialidases or other enzymes essential for sialic acid scavenging in other Firmicutes, is evidence that variation in specific activity of the enzyme is perpetuated by a nonnutritive function in M. synoviae that is influenced by the genomic context of the organism.

* Corresponding author. Mailing address: Department of Infectious Diseases and Pathology, College of Veterinary Medicine, University of Florida, Gainesville, FL 32611-0880. Phone: (352) 392-2239, ext. 3975. Fax: (352) 392-9704. E-mail: BrownD{at}vetmed.ufl.edu

{triangledown} Published ahead of print on 27 March 2009.

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

Journal of Bacteriology, June 2009, p. 3588-3593, Vol. 191, No. 11
0021-9193/09/$08.00+0     doi:10.1128/JB.00142-09
Copyright © 2009, American Society for Microbiology. All Rights Reserved.





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