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Disruption of coding regions by IS6110 insertion in Mycobacterium tuberculosis
S L Sampson1, R M Warren, M Richardson
1Department of Medical Biochemistry, University of Stellenbosch Medical School, Tygerberg.
Tubercle and Lung Disease : the Official Journal of the International Union Against Tuberculosis and Lung Disease
|March 1, 2000
Summary
The insertion sequence IS6110 is found at 66 unique locations in the Mycobacterium tuberculosis genome, often disrupting genes. While these disruptions may not significantly alter bacterial phenotype, they offer insights into Mycobacterium tuberculosis evolution.
Area of Science:
- Microbiology
- Genomics
- Molecular Biology
Background:
- The insertion sequence IS6110 is a key tool for DNA fingerprinting and classifying Mycobacterium tuberculosis strains.
- Understanding IS6110 insertion patterns is crucial for studying the genetic diversity and evolution of M. tuberculosis.
Purpose of the Study:
- To characterize the genomic location and genetic identity of IS6110 insertion sites in clinical M. tuberculosis isolates.
- To investigate whether IS6110 transposition events contribute to phenotypic changes in M. tuberculosis.
Main Methods:
- Cloning of 33 IS6110 insertion loci from 8 clinical M. tuberculosis isolates.
- Identification of DR locus insertions via hybridization and characterization of other loci through DNA sequencing.
- Analysis of sequence data combined with published literature and DNA sequence databases.
Main Results:
- Analysis of 76 sequences revealed 66 unique IS6110 insertion loci across the M. tuberculosis genome.
- The majority of unique loci (42) disrupted coding regions, including insertions into the ipl locus.
- Insertions were distributed throughout the chromosome, with some evidence of preferential insertion sites.
Conclusions:
- The study identified 66 unique IS6110 insertion loci dispersed in the M. tuberculosis genome.
- A high incidence of IS6110 insertions within coding regions was observed.
- The impact of these IS6110-mediated coding region disruptions on bacterial phenotype may be limited due to gene family redundancy.