A group of gram-negative bacteria responsible for bubonic plague (characterized by enlarged lymph nodes [bubo]), gastroenteritis, etc. in rodents and humans acquired through fleabites. Generally, but not always, infectiveness of the flea carriers may be blocked during the early stages of the incubation period (Eisen RJ et al 2006 Proc Natl Acad Sci USA 103:15380). The sequenced genome of Y. pestis includes a 4.65 Mb chromosome and three plasmids of 96.2, 70.3 and 9.6 kb. It contains 150 pseudogenes. The genome shows frequent insertion sequences and intragenic recombinations. The bacteria secrete the Yop protein that targets primarily dendritic cells, macrophages and neutrophils of the immune system but rarely the B and T lymphocytes (Marketon MM et al 2005 Science 309:1739). YopJ acetylates and inhibits MAPK kinase activation and inhibits NF-κB signaling, thus disarming the innate immune system. YopJ acts as an acetyltransferase, using acetyl-CoA, and modifies critical serine and threonine residues in the activation loop of MAPKK6 and prevents phosphorylation (Mukherjee S et al 2006 Science 312:1211). Yersinia protein kinase A (YpkA) disrupts the eukaryotic actin cytoskeleton. Its Rac1 binding domain mimics the host guanidine nucleotide dissociation inhibitors of Rho GTPases (Prehna G et al 2006 Cell 126:869). Pneumonic plague development requires the presence of plasminogen-activating protease (Lathem WW et al 2007 Science 315:509). virulence, biological weapons, plague, plant vaccines, herpes, cytoskeleton, Rac, RHO; Parkhill J et al 2001 Nature [Lond] 413:323; Hinnebusch BJ et al 2002 Science 296:733; Cornelis GR 2002 Nature Rev Mol Cell Biol 3:742; genome: http://bbrp.llnl.gov/bbrp/html/microbe.html.
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