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Chapter 70 : The Role of the Phagosomal Transporter (Pht) Family of Proteins in Pathogenesis

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The Role of the Phagosomal Transporter (Pht) Family of Proteins in Pathogenesis, Page 1 of 2

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Abstract:

A central aspect of the pathogenesis of is its ability to differentiate in response to nutrient availability. The phagosomal transporter (Pht) proteins are members of the major facilitator superfamily of proteins which are ATP-independent transporters that perform diverse functions in both prokaryotic and eukaryotic cells. One of these transporters, PhtA, is required by intracellular for threonine acquisition, differentiation, and growth. Accordingly, the authors have developed a model in which Pht proteins are responsible for acquisition of nutrients in the nascent phagosome; have postulated that this process is absolutely required both for differentiation and growth within host macrophages. Knowing that nutrient starvation in broth triggers differentiation of replicative cells to the transmissive form, the authors tested if threonine limitation, caused by mutation of the locus, impaired differentiation of intracellular bacteria. Analysis of mutants that lack one of each of the other members of the Pht family indicated that some of the putative transporters are required for growth within mouse macrophages, but others are not. In particular, the , , , genes are not essential for growth within macrophages, while , , , , and are required for replication.

Citation: Sauer J, S. Swanson M. 2006. The Role of the Phagosomal Transporter (Pht) Family of Proteins in Pathogenesis, p 288-291. In Cianciotto N, Kwaik Y, Edelstein P, Fields B, Geary D, Harrison T, Joseph C, Ratcliff R, Stout J, Swanson M (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555815660.ch70

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Major Facilitator Superfamily
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Amino Acids
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Figures

Image of FIGURE 1
FIGURE 1

Model of Pht function in intracellular differentiation and replication. In the proposed intracellular model of differentiation, we believe that the Pht family of transporters plays a central role in the differentiation from the transmissive form to the replicative form following internalization of . Recognition of rich intracellular stores of nutrients via the Pht transporters allows release of the stringent response and the subsequent differentiation to the replicative form as a prerequisite for intracellular growth. Upon exhaustion of nutrients, the stringent response triggers differentiation back to the transmissive form.

Citation: Sauer J, S. Swanson M. 2006. The Role of the Phagosomal Transporter (Pht) Family of Proteins in Pathogenesis, p 288-291. In Cianciotto N, Kwaik Y, Edelstein P, Fields B, Geary D, Harrison T, Joseph C, Ratcliff R, Stout J, Swanson M (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555815660.ch70
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Image of FIGURE 2
FIGURE 2

Pht family phylogeny. Clustal W alignment of the protein sequences of the Philadelphia 1 strain indicates the relation of the Pht family of proteins to one another. Analysis of growth of mutants shows that some Phts are required for growth within A/J mouse bone marrow-derived macrophages while others are not. PhtA and PhtJ are most likely threonine and valine transporters, respectively.

Citation: Sauer J, S. Swanson M. 2006. The Role of the Phagosomal Transporter (Pht) Family of Proteins in Pathogenesis, p 288-291. In Cianciotto N, Kwaik Y, Edelstein P, Fields B, Geary D, Harrison T, Joseph C, Ratcliff R, Stout J, Swanson M (ed), . ASM Press, Washington, DC. doi: 10.1128/9781555815660.ch70
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References

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1. Bachman, M. A., and, M. S. Swanson. 2001. RpoS co-operates with other factors to induce Legionella pneumophila virulence in the stationary phase. Mol. Microbiol. 40:12011214.
2. Byrne, B., and, M. S. Swanson. 1998. Expression of Legionella pneumophila virulence traits in response to growth conditions. Infect. Immun. 66:30293034.
3. Hammer, B. K., and, M. S. Swanson. 1999. Co-ordination of Legionella pneumophila virulence with entry into stationary phase by ppGpp. Mol. Microbiol. 33:721731.
4. Hammer, B. K.,, E. S. Tateda, and, M. S. Swan-son. 2002. A two-component regulator induces the transmission phenotype of stationary-phase Le-gionella pneumophila. Mol. Microbiol. 44:107118.
5. Harb, O. S., and, Y. Abu Kwaik. 2000. Characterization of a macrophage-specific infectivity locus (milA) of Legionella pneumophila. Infect. Immun. 68:368376.
6. Jacobi, S.,, R. Schade, and, K. Heuner. 2004. Characterization of the alternative sigma factor sigma54 and the transcriptional regulator FleQ of Legionella pneumophila, which are both involved in the regulation cascade of flagellar gene expression. J. Bacteriol. 186:25402547.
7. Molofsky, A. B., and, M. S. Swanson. 2003. Le-gionella pneumophila CsrA is a pivotal repressor of transmission traits and activator of replication. Mol. Microbiol. 50:445461.
8. Oyston, P. C.,, A. Sjostedt, and, R. W. Titball. 2004. Tularaemia: bioterrorism defence renews interest in Francisella tularensis. Nat. Rev. Microbiol. 2:967978.
9. Pao, S. S.,, I. T. Paulsen, and, M. H. Saier, Jr. 1998. Major facilitator superfamily. Microbiol. Mol. Biol. Rev. 62:134.
10. Sauer, J. D.,, M. A. Bachman, and, M. S. Swan-son. 2005. The phagosomal transporter A couples threonine acquisition to differentiation and replication of Legionella pneumophila in macrophages. Proc. Natl. Acad. Sci. USA 102:99249929.

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