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Infection and Immunity, September 1999, p. 4551-4556, Vol. 67, No. 9
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
The Autolysin-Encoding Gene (lytA) of
Streptococcus pneumoniae Displays Restricted Allelic
Variation despite Localized Recombination Events with Genes of
Pneumococcal Bacteriophage Encoding Cell Wall Lytic
Enzymes
Adrian M.
Whatmore* and
Christopher G.
Dowson
Department of Biological Sciences, University
of Warwick, Coventry CV4 7AL, United Kingdom
Received 15 March 1999/Returned for modification 4 May
1999/Accepted 1 June 1999
The lytA-encoded autolysin
(N-acetylmuramoyl-L-alanine amidase) of
Streptococcus pneumoniae is believed to play an important role in the pathogenesis of pneumococcal infection and has been identified as a putative vaccine target. Allelic diversity of lytA in an extensive collection of clinical isolates was
assessed by restriction fragment length polymorphism and confirmatory
sequencing studies. Genetic diversity within lytA is
limited, especially compared to the high levels of diversity seen in
other pneumococcal virulence factor genes, although small blocks
generating mosaic structure were identified. Sequence comparisons with
genes encoding cell wall lytic enzymes of pneumococcal bacteriophage
suggest that localized recombination events have occurred between host lytA and these bacteriophage genes. These results confirm
earlier suggestions that recombination between DNA encoding
bacteriophage autolytic enzymes and chromosomally encoded
lytA might be important in the evolution of
lytA. The implications of these findings for understanding
the evolution of lytA and the potential utility of LytA as
a vaccine target are discussed.
*
Corresponding author. Mailing address: Department of
Biological Sciences, University of Warwick, Coventry, CV4 7AL, United Kingdom. Phone: 44 1203 528359. Fax: 44 1203 523701. E-mail:
a.m.whatmore{at}warwick.ac.uk.
Infection and Immunity, September 1999, p. 4551-4556, Vol. 67, No. 9
0019-9567/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.
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