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The Yersinia high-pathogenicity island (HPI): evolutionary and functional aspects
Sören Schubert1, Alexander Rakin, Jürgen Heesemann
1Max von Pettenkofer-Institut für Hygiene und Medizinische Mikrobiologie, Lehrstuhl für Bakteriologie, Pettenkoferstr 9a, D-80336 München, Germany.
International Journal of Medical Microbiology : IJMM
|October 21, 2004
Summary
The high-pathogenicity island (HPI) is crucial for Yersinia and E. coli virulence. This genomic island can transfer via conjugation, potentially as an integrative and conjugative element (ICE), spreading pathogenicity.
Area of Science:
- Microbiology
- Genomics
- Molecular Biology
Background:
- The high-pathogenicity island (HPI) is a mobile genetic element critical for virulence in Yersinia species and certain Escherichia coli pathotypes.
- Unlike most genomic islands, HPI is widely distributed within the Enterobacteriaceae family.
Purpose of the Study:
- To elucidate the genetic makeup and mobility mechanisms of the high-pathogenicity island.
- To understand the role of HPI in bacterial fitness and pathogenicity.
- To investigate the conjugative transfer of HPI, particularly in E. coli.
Main Methods:
- Bioinformatic analysis of HPI genetic components.
- Characterization of HPI integration and excision mechanisms.
- Investigation of HPI transfer in E. coli strain ECOR31, including its potential as an integrative and conjugative element (ICE).
Main Results:
- HPI encodes a mobility module (integrase, excisionase) and a functional part for yersiniabactin biosynthesis and uptake.
- HPI integrates into specific asn tRNA genes (attB sites) in Yersinia pestis and E. coli.
- A unique HPI in E. coli ECOR31 exhibits characteristics of an ICE, suggesting a conjugative transfer mechanism.
Conclusions:
- The HPI possesses a sophisticated genetic system for integration, excision, and dissemination.
- Conjugative transfer, potentially as an ICE (ICEEcl), is a proposed mechanism for HPI spread among Enterobacteriaceae.
- Understanding HPI mobility is key to comprehending bacterial pathogenicity and evolution.