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Infection and Immunity, August 2004, p. 4503-4511, Vol. 72, No. 8
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.8.4503-4511.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.

A Specific Genomic Location within the icm/dot Pathogenesis Region of Different Legionella Species Encodes Functionally Similar but Nonhomologous Virulence Proteins

Michal Feldman and Gil Segal*

Department of Molecular Microbiology and Biotechnology, George S. Wise Faculty of Life Sciences, Tel-Aviv University, Ramat-Aviv, Tel-Aviv 69978, Israel

Received 26 February 2004/ Returned for modification 26 April 2004/ Accepted 6 May 2004

Legionella pneumophila, the major causative agent of Legionnaires' disease, is a facultative intracellular pathogen that grows within human macrophages and amoebae. Intracellular growth involves the formation of a replicative phagosome that requires the Icm/Dot type IV secretion system. Part of the icm/dot region in L. pneumophila contains the icmTSRQPO genes. The proteins encoded by the icmR and icmQ genes were shown to exhibit a chaperone-substrate relationship. Analysis of this region from other pathogenic Legionella species, i.e., L. micdadei and L. longbeachae, indicated that the overall organization of this region is highly conserved, but it was found to contain a favorable site for gene variation. In the place where the icmR gene was expected to be located, other open reading frames that are nonhomologous to each other or to any entry in the GenBank database were found (migAB in L. micdadei and ligB in L. longbeachae). Examination of these unique genes revealed an outstanding phenomenon; by use of interspecies complementation, the icmR, migB, and ligB gene products were found to be functionally similar. In addition, the function of these proteins was usually dependent on the presence of the corresponding IcmQ proteins. Moreover, each of these proteins (IcmR, LigB, and MigB) was found to interact with the corresponding IcmQ proteins, and the genes encoding these proteins were found to be regulated by CpxR. This study reveals new evidence of gene variation occurring in the same genomic location within the icm/dot locus in various Legionella species. The genes found at this site were shown to be similarly regulated and to encode species-specific, nonhomologous, but functionally similar proteins.

* Corresponding author. Mailing address: Department of Molecular Microbiology and Biotechnology, George S. Wise Faculty of Life Sciences, Tel-Aviv University, Ramat-Aviv, Tel-Aviv 69978, Israel. Phone: 972-3-6405287. Fax: 972-3-6409407. E-mail: gils{at}tauex.tau.ac.il.

Editor: J. T. Barbieri

Infection and Immunity, August 2004, p. 4503-4511, Vol. 72, No. 8
0019-9567/04/$08.00+0     DOI: 10.1128/IAI.72.8.4503-4511.2004
Copyright © 2004, American Society for Microbiology. All Rights Reserved.



This article has been cited by other articles:

  • Zusman, T., Degtyar, E., Segal, G. (2008). Identification of a Hypervariable Region Containing New Legionella pneumophila Icm/Dot Translocated Substrates by Using the Conserved icmQ Regulatory Signature. Infect. Immun. 76: 4581-4591 [Abstract] [Full Text]  
  • Herbert, E. E., Cowles, K. N., Goodrich-Blair, H. (2007). CpxRA Regulates Mutualism and Pathogenesis in Xenorhabdus nematophila. Appl. Environ. Microbiol. 73: 7826-7836 [Abstract] [Full Text]  
  • Feldman, M., Segal, G. (2007). A Pair of Highly Conserved Two-Component Systems Participates in the Regulation of the Hypervariable FIR Proteins in Different Legionella Species. J. Bacteriol. 189: 3382-3391 [Abstract] [Full Text]  
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  • Newton, H. J., Sansom, F. M., Bennett-Wood, V., Hartland, E. L. (2006). Identification of Legionella pneumophila-Specific Genes by Genomic Subtractive Hybridization with Legionella micdadei and Identification of lpnE, a Gene Required for Efficient Host Cell Entry. Infect. Immun. 74: 1683-1691 [Abstract] [Full Text]  
  • Feldman, M., Zusman, T., Hagag, S., Segal, G. (2005). Coevolution between nonhomologous but functionally similar proteins and their conserved partners in the Legionella pathogenesis system. Proc. Natl. Acad. Sci. USA 102: 12206-12211 [Abstract] [Full Text]  


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