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Characterization of a Pathogenic Escherichia coli Strain Derived from Oreochromis spp. Farms Using Whole-Genome Sequencing

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Centromere anatomy in the multidrug-resistant pathogen Enterococcus faecium.

Andrew Derome¹, Christian Hoischen, Malte Bussiek

¹Faculty of Life Sciences and Manchester Interdisciplinary Biocentre, University of Manchester, Manchester M1 7DN, United Kingdom.

Proceedings of the National Academy of Sciences of the United States of America

|February 5, 2008

Summary

This summary is machine-generated.

Researchers identified key genes and DNA sequences involved in the segregation of high-level gentamicin-resistance plasmids in Enterococcus. Understanding these mechanisms could help combat antibiotic resistance in hospital-acquired infections.

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Area of Science:

Microbiology
Molecular Biology
Genetics

Background:

Multidrug-resistant Enterococcus strains are a major cause of hospital-acquired infections.
Plasmid-borne resistance genes drive antibiotic resistance evolution in enterococci.

Purpose of the Study:

To identify and dissect the segregation locus of a high-level gentamicin-resistance plasmid (pGENT) in Enterococcus faecium.
To understand the molecular mechanisms of plasmid segregation in enterococci.

Main Methods:

Genetic dissection of the pGENT plasmid's segregation locus.
Identification of genes PrgP (ParA superfamily) and PrgO (DNA binding protein).
Atomic force microscopy and DNA bending analysis to study the centromere (cenE) and PrgO interaction.

Main Results:

The segregation locus contains overlapping genes PrgP and PrgO.
PrgO binds the distinctive cenE centromere, with three subsites (CESI, CESII, CESIII) containing TATA boxes.
PrgO binding is asymmetric, and cenE is intrinsically curved, potentially mirroring yeast centromere organization.

Conclusions:

The identified segregation mechanism involving PrgP and PrgO is crucial for pGENT plasmid stability.
Homologous segregation modules are widespread on other resistance plasmids in enterococci.
Understanding segrosome assembly may offer new strategies against antibiotic resistance in Enterococcus.