共 43 条
SpiC is required for translocation of Salmonella pathogenicity island 2 effectors and secretion of translocon proteins SseB and SseC
被引:71
作者:

Freeman, JA
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机构: Univ Washington, Dept Microbiol, Seattle, WA 98195 USA

Rappl, C
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机构: Univ Washington, Dept Microbiol, Seattle, WA 98195 USA

Kuhle, V
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机构: Univ Washington, Dept Microbiol, Seattle, WA 98195 USA

Hensel, M
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机构: Univ Washington, Dept Microbiol, Seattle, WA 98195 USA

Miller, SI
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机构: Univ Washington, Dept Microbiol, Seattle, WA 98195 USA
机构:
[1] Univ Washington, Dept Microbiol, Seattle, WA 98195 USA
[2] Univ Washington, Dept Med, Seattle, WA 98195 USA
[3] Univ Munich, Lehrstuhl Bakteriol, Max Von Pettenkofer Inst Hyg & Med Mikrobiol, Munich, Germany
[4] FAu Erlangen Nurnberg, Inst Klin Mikrobiol Immunol & Hyg, Erlangen, Germany
关键词:
D O I:
10.1128/JB.184.18.4971-4980.2002
中图分类号:
Q93 [微生物学];
学科分类号:
071005 ;
100705 ;
摘要:
The Salmonella pathogenicity island 2 (SPI2) type III secretion system (TTSS) promotes Salmonella enterica serovar Typhimurium virulence for mice and increased survival and replication within eukaryotic cells. After phagocytosis, Salmonella serovar Typhimurium assembles the SPI2 TTSS to translocate over a dozen effector proteins across the phagosome membrane. SpiC has been previously shown to be a translocated effector with a large contribution to virulence (K. Uchiya, M. A. Barbieri, K. Funato, A. H. Shah, P. D. Stahl, and E. A. Groisman, EMBO J. 18:3924-3933, 1999). This report demonstrates by competitive index that the virulence phenotype of a spiC mutant is equivalent to that of a secretion component mutant. In addition, translocation of SPI2 effector proteins was shown to require SpiC. Thus, the severe virulence phenotype resulting from deletion of spiC is likely due to the inability to translocate all SPI2 effectors. SpiC was also required to secrete translocon proteins SseB and SseC but not translocated effector SseJ, indicating that lack of assembly of the translocon explains the spiC mutant phenotype.
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页码:4971 / 4980
页数:10
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