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Chapter 18 : Genetic Analysis of Intracellular Multiplication in Human and Protozoan Hosts

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Genetic Analysis of Intracellular Multiplication in Human and Protozoan Hosts, Page 1 of 2

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Abstract:

Several approaches have been taken to understand the genetic basis for intracellular multiplication by . The first was based on the properties of avirulent variants that had lost the ability to replicate inside macrophages and were also defective in preventing phagosome-lysosome fusion. Researchers reasoned that introduction of a wild-type region of the genome that restored the ability to replicate within and kill human macrophages would provide information about the genes that were defective in the variants. A genomic library of wild-type DNA was introduced to one of the avirulent variants, and complemented bacteria that regained the abilities to replicate intracellularly and kill host cells were identified with the aid of a plaque assay. The striking homology between the / genes and the IncI and genes involved in conjugal DNA transfer prompted us to examine if could conjugally transfer DNA. The current model for how the Icm/Dot complex influences the intracellular fate of postulates that there are two classes of Icm/Dot gene products. Several possible mechanisms could be used to specifically interrupt the fusion of phagosomes with lysosomes.

Citation: Segal G, Shuman H. 2002. Genetic Analysis of Intracellular Multiplication in Human and Protozoan Hosts, p 90-96. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch18

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Type IV Secretion Systems
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Figures

Image of FIGURE 1
FIGURE 1

Linkage map of the two regions. Region I contains and region II contains . Coding regions are indicated by bold arrows. The homologs from the IncI plasmid colIb-P9 are indicated under the corresponding gene. Shading indicates the predicted location of the protein in the bacterial cell: , lipoprotein; , cytoplasm; inner membrane; periplasm. The star indicates genes that were found to have homologs in .

Citation: Segal G, Shuman H. 2002. Genetic Analysis of Intracellular Multiplication in Human and Protozoan Hosts, p 90-96. In Marre R, Abu Kwaik Y, Bartlett C, Cianciotto N, Fields B, Frosch M, Hacker J, Lück P (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555817985.ch18
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References

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1. Berger, K. H.,, J. J. Merriam,, and R. R. Isberg. 1994. Altered intracellular targeting properties associated with mutations in the Legionella dotA gene. Mol. Microbiol. 14: 809 822.
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3. Marra, A.,, S. J. Blander,, M. A. Horwitz,, and H. A. Shuman. 1992. Identification of a Legionella pneumophila locus required for intracellular multiplication in human macrophages. Proc. Natl. Acad. Sci. USA 89: 9607 9611.
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8. Segal, G.,, J. J. Russo,, and H. A. Shuman. 1999. Relationships between a new type IV secretion system and the km/dot virulence system of Legionella pneumophila. Mol. Microbiol. 34: 799 809.
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10. Segal, G.,, and H. A. Shuman. 1998. Intracellular multiplication and human macrophage killing by Legionella pneumophila are inhibited by conjugal components of IncQ plasmid RSF1010. Mol. Miaobiol. 30: 197 208.
11. Segal, G.,, and H. A. Shuman. 1999. Legionella pneumophila utilizes the same genes to multiply within Acanthamoeba castellanii and human macrophages. Infect. Immun. 67: 2117 2124.
12. Vogel, J. P.,, H. L. Andrews,, S. K. Wong,, and R. R. Isberg. 1998. Conjugative transfer by the virulence system of Legionella pneumophila. Science 279: 873 876.
13. Wiater, L. A.,, K. Dunn,, F. R. Maxfield,, and H. A. Shuman. 1998. Early events in phagosome establishment are required for intracellular survival of Legionella pneumophila. Infect. Immun. 66: 4450 4460.
14. Winans, S. C.,, D. L. Bums,, and P.J. Christie. 1996. Adaptation of the conjugal transfer system for the export of pathogenic macromolecules. Trends Microbiol. 4: 64 68.

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