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Total Protein Extraction and 2-D Gel Electrophoresis Methods for Burkholderia Species
Published on: October 15, 2013
Genomic islands from five strains of Burkholderia pseudomallei
Apichai Tuanyok1, Benjamin R Leadem, Raymond K Auerbach
1Department of Biological Sciences, Northern Arizona University, Flagstaff, AZ 86011-5640, USA. Apichai.Tuanyok@nau.edu
Background:
Burkholderia pseudomallei is the etiologic agent of melioidosis, a significant cause of morbidity and mortality where this infection is endemic. Genomic differences among strains of B. pseudomallei are predicted to be one of the major causes of the diverse clinical manifestations observed among patients with melioidosis. The purpose of this study was to examine the role of genomic islands (GIs) as sources of genomic diversity in this species.
Results:
We found that genomic islands (GIs) vary greatly among B. pseudomallei strains. We identified 71 distinct GIs from the genome sequences of five reference strains of B. pseudomallei: K96243, 1710b, 1106a, MSHR668, and MSHR305. The genomic positions of these GIs are not random, as many of them are associated with tRNA gene loci. In particular, the 3' end sequences of tRNA genes are predicted to be involved in the integration of GIs. We propose the term "tRNA-mediated site-specific recombination" (tRNA-SSR) for this mechanism. In addition, we provide a GI nomenclature that is based upon integration hotspots identified here or previously described.
Conclusion:
Our data suggest that acquisition of GIs is one of the major sources of genomic diversity within B. pseudomallei and the molecular mechanisms that facilitate horizontally-acquired GIs are common across multiple strains of B. pseudomallei. The differential presence of the 71 GIs across multiple strains demonstrates the importance of these mobile elements for shaping the genetic composition of individual strains and populations within this bacterial species.
Insights
Genomic islands (GIs) significantly contribute to the diversity of Burkholderia pseudomallei, the bacteria causing melioidosis. Researchers identified 71 GIs, revealing common integration mechanisms across strains.
Area of Science:
- Microbiology
- Genomics
- Bacterial Pathogenesis
Background:
- Burkholderia pseudomallei causes melioidosis, a disease with significant morbidity and mortality in endemic areas.
- Genomic variations among B. pseudomallei strains are linked to diverse clinical presentations.
- Genomic islands (GIs) are key contributors to bacterial genome diversity.
Purpose of the Study:
- To investigate the role of genomic islands (GIs) in driving genomic diversity within Burkholderia pseudomallei.
- To understand the mechanisms underlying GI acquisition and their impact on strain variation.
Main Methods:
- Comparative analysis of genome sequences from five reference B. pseudomallei strains.
- Identification and characterization of distinct genomic islands (GIs).
- Mapping GI locations and identifying potential integration sites, particularly tRNA gene loci.
Main Results:
- Seventy-one distinct genomic islands (GIs) were identified across the five reference B. pseudomallei strains.
- GIs were frequently associated with tRNA gene loci, suggesting a role in their integration.
- A novel mechanism, "tRNA-mediated site-specific recombination" (tRNA-SSR), was proposed for GI integration.
- A nomenclature for GIs based on integration hotspots was established.
Conclusions:
- The acquisition of genomic islands (GIs) is a primary driver of genomic diversity in B. pseudomallei.
- The molecular mechanisms facilitating the horizontal acquisition of GIs are conserved across multiple B. pseudomallei strains.
- The variable distribution of GIs highlights their importance in shaping the genetic makeup of B. pseudomallei populations.
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