Journal of Bacteriology, March 2004, p. 1818-1832, Vol. 186, No. 6
0021-9193/04/$08.00+0 DOI: 10.1128/JB.186.6.1818-1832.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
The pKO2 Linear Plasmid Prophage of Klebsiella oxytoca
Sherwood R. Casjens,1,2* Eddie B. Gilcrease,1 Wai Mun Huang,1 Kim L. Bunny,3 Marisa L. Pedulla,2,4 Michael E. Ford,2,4 Jennifer M. Houtz,2,4 Graham F. Hatfull,2,4 and Roger W. Hendrix2,4
Department of Pathology, University of Utah Medical School, Salt Lake City, Utah 84132,1
Pittsburgh Bacteriophage Institute,2
Department of Biological Sciences, University of Pittsburgh, Pittsburgh, Pennsylvania 15260,4
Section of Microbiology, University of California at Davis, Davis, California 956163
Received 16 September 2003/
Accepted 10 December 2003
Temperate bacteriophages with plasmid prophages are uncommon in nature, and of these only phages N15 and PY54 are known to have a linear plasmid prophage with closed hairpin telomeres. We report here the complete nucleotide sequence of the 51,601-bp Klebsiella oxytoca linear plasmid pKO2, and we demonstrate experimentally that it is also a prophage. We call this bacteriophage
KO2. An analysis of the 64 predicted
KO2 genes indicate that it is a fairly close relative of phage N15; they share a mosaic relationship that is typical of different members of double-stranded DNA tailed-phage groups. Although the head, tail shaft, and lysis genes are not recognizably homologous between these phages, other genes such as the plasmid partitioning, replicase, prophage repressor, and protelomerase genes (and their putative targets) are so similar that we predict that they must have nearly identical DNA binding specificities. The
KO2 virion is unusual in that its phage
-like tails have an exceptionally long (3,433 amino acids) central tip tail fiber protein. The
KO2 genome also carries putative homologues of bacterial dinI and umuD genes, both of which are involved in the host SOS response. We show that these divergently transcribed genes are regulated by LexA protein binding to a single target site that overlaps both promoters.
* Corresponding author. Mailing address: Department of Pathology, University of Utah Medical School, Salt Lake City, UT 84132. Phone: (801) 581-5980. Fax: (801) 581-3607. E-mail: sherwood.casjens{at}path.utah.edu.
Journal of Bacteriology, March 2004, p. 1818-1832, Vol. 186, No. 6
0021-9193/04/$08.00+0 DOI: 10.1128/JB.186.6.1818-1832.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.
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Copyright © 2004 by the American Society for Microbiology. All rights reserved.