Co-evolution and exploitation of host cell signaling pathways by bacterial pathogens

被引:35
作者
Shames, Stephanie R. [1 ,2 ]
Auweter, Sigrid D. [1 ]
Finlay, B. Brett [1 ,2 ]
机构
[1] Univ British Columbia, Michael Smith Labs, Vancouver, BC V6T 1Z4, Canada
[2] Univ British Columbia, Dept Microbiol & Immunol, Vancouver, BC V6T 1Z4, Canada
基金
瑞士国家科学基金会;
关键词
Bacterial pathogen; Mimicry; Innate immunity; Evolution; Effector protein; E3 UBIQUITIN LIGASE; NF-KAPPA-B; ACTIN CYTOSKELETON REARRANGEMENTS; PHOSPHOTHREONINE LYASE ACTIVITY; ACTIVATED PROTEIN-KINASES; III SECRETION SYSTEM; ESCHERICHIA-COLI; EFFECTOR PROTEIN; PHOSPHOINOSITIDE METABOLISM; SALMONELLA EFFECTOR;
D O I
10.1016/j.biocel.2008.08.013
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Bacterial pathogens have evolved by combinations of gene acquisition, deletion, and modification, which increases their fitness. Additionally, bacteria are able to evolve in "quantum leaps" via the ability to promiscuously acquire new genes. Many bacterial pathogens - especially Gram-negative enteric pathogens - have evolved mechanisms by which to subvert signal transduction pathways of eukaryotic cells by expressing genes that mimic or regulate host protein factors involved in a variety of signaling cascades. This results in the ability to cause diseases ranging from tumor formation in plants to gastroenteritis and bubonic plague. Here, we present recent advances on mechanisms of bacterial pathogen evolution, including specific signaling cascades targeted by their virulence genes with an emphasis on the ubiquitin modification system, Rho GTPase regulators, cytoskeletal modulators, and host innate immunity. We also comment briefly on evolution of host defense mechanisms in place that limit disease caused by bacterial pathogens. (c) 2008 Elsevier Ltd. All rights reserved.
引用
收藏
页码:380 / 389
页数:10
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