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Effector Translocation by the Legionella Dot/Icm Type IV Secretion System

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Molecular Mechanisms in Legionella Pathogenesis

Part of the book series: Current Topics in Microbiology and Immunology ((CT MICROBIOLOGY,volume 376))

Abstract

Legionella pneumophila is an opportunistic pathogen responsible for Legionnaires’ disease. This bacterium survives and replicates within phagocytes by bypassing their bactericidal activity. Intracellular replication of L. pneumophila requires the Dot/Icm type IV secretion system made of approximately 27 proteins that presumably traverses the bacterial and phagosomal membranes. The perturbation of the host killing ability largely is mediated by the collective functions of the protein substrates injected into host cells via the Dot/Icm transporter. Proper protein translocation by Dot/Icm is determined by a number of factors, including signals recognizable by the translocator, chaperones that may facilitate the proper folding of substrates and transcriptional regulation and protein stability that determine the abundance and temporal transfer of the substrates. Although a large number of Dot/Icm substrates have been identified, investigation to understand the translocation is ongoing. Here we summarized the recent advancements in our understanding of the factors that determine the protein translocation activity of the Dot/Icm transporter.

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Abbreviations

Dot/Icm:

Defective in organelle trafficking/intracellular multiplication)

Arf:

ADP ribosylation factor

GEFs:

Guanine nucleotide exchange factors

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Acknowledgments

We thank Dr. Xiaodi Niu (Jilin University, Changchun, China) for help in the preparation of the figure and members of our laboratory for helpful discussion. Our work was supported by NIH-NIAID grants R01AI069344, K02AI085403 and R21AI092043.

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Correspondence to Zhao-Qing Luo .

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© 2013 Springer-Verlag Berlin Heidelberg

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Qiu, J., Luo, ZQ. (2013). Effector Translocation by the Legionella Dot/Icm Type IV Secretion System. In: Hilbi, H. (eds) Molecular Mechanisms in Legionella Pathogenesis. Current Topics in Microbiology and Immunology, vol 376. Springer, Berlin, Heidelberg. https://doi.org/10.1007/82_2013_345

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