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Generation of Enterobacter sp. YSU Auxotrophs Using Transposon Mutagenesis
Published on: October 31, 2014
The virulence plasmid of Yersinia, an antihost genome
G R Cornelis1, A Boland, A P Boyd
1Microbial Pathogenesis Unit, Christian de Duve Institute of Cellular Pathology and Faculté de Médecine, Université Catholique de Louvain, B-1200 Brussels, Belgium. cornelis@mipa.ucl.ac.be
Abstract:
The 70-kb virulence plasmid enables Yersinia spp. (Yersinia pestis, Y. pseudotuberculosis, and Y. enterocolitica) to survive and multiply in the lymphoid tissues of their host. It encodes the Yop virulon, an integrated system allowing extracellular bacteria to disarm the cells involved in the immune response, to disrupt their communications, or even to induce their apoptosis by the injection of bacterial effector proteins. This system consists of the Yop proteins and their dedicated type III secretion apparatus, called Ysc. The Ysc apparatus is composed of some 25 proteins including a secretin. Most of the Yops fall into two groups. Some of them are the intracellular effectors (YopE, YopH, YpkA/YopO, YopP/YopJ, YopM, and YopT), while the others (YopB, YopD, and LcrV) form the translocation apparatus that is deployed at the bacterial surface to deliver the effectors into the eukaryotic cells, across their plasma membrane. Yop secretion is triggered by contact with eukaryotic cells and controlled by proteins of the virulon including YopN, TyeA, and LcrG, which are thought to form a plug complex closing the bacterial secretion channel. The proper operation of the system also requires small individual chaperones, called the Syc proteins, in the bacterial cytosol. Transcription of the genes is controlled both by temperature and by the activity of the secretion apparatus. The virulence plasmid of Y. enterocolitica and Y. pseudotuberculosis also encodes the adhesin YadA. The virulence plasmid contains some evolutionary remnants including, in Y. enterocolitica, an operon encoding resistance to arsenic compounds.
Insights
The Yersinia virulence plasmid and its Yop virulon system allow bacteria to inject effector proteins into host immune cells, aiding survival. This complex type III secretion system (Ysc) is crucial for Yersinia pathogenesis.
Area of Science:
- Microbiology
- Immunology
- Molecular Biology
Background:
- Yersinia spp. possess a 70-kb virulence plasmid essential for survival in host lymphoid tissues.
- The plasmid encodes the Yop virulon, a sophisticated system for bacterial pathogenesis.
- This system facilitates the injection of effector proteins into host immune cells.
Purpose of the Study:
- To elucidate the molecular mechanisms of the Yop virulon and its type III secretion system (Ysc).
- To understand how Yersinia spp. manipulate host immune responses.
- To detail the protein components and regulatory aspects of the Ysc apparatus.
Main Methods:
- Analysis of the Yop virulon components, including effector proteins (YopE, YopH, etc.) and translocation apparatus proteins (YopB, YopD, LcrV).
- Investigation of the type III secretion apparatus (Ysc) structure and function.
- Examination of regulatory proteins (YopN, TyeA, LcrG) and chaperones (Syc proteins) involved in Yop secretion.
Main Results:
- The Yop virulon comprises intracellular effectors and a surface-deployed translocation apparatus.
- Yop secretion is triggered by host cell contact and regulated by specific protein complexes.
- The Ysc apparatus, composed of ~25 proteins, facilitates effector delivery across the host cell membrane.
- Additional virulence factors like YadA and arsenic resistance operons are encoded on the plasmid.
Conclusions:
- The Yop virulon and Ysc system are critical for Yersinia virulence, enabling immune evasion and host cell manipulation.
- The intricate regulation of Yop secretion highlights a highly evolved pathogenic strategy.
- The virulence plasmid harbors diverse genetic elements contributing to bacterial survival and pathogenicity.
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