Bidirectional deletions associated with IS4

Habermann, P.; Starlinger, Peter

doi:10.1007/bf00330790

Cited by 10 publications

(3 citation statements)

References 31 publications

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“…Associated with mini-IS605 in this strain was a deletion that removed 462 bp of rdxA. Several different IS elements that are not related to IS605 or mini-IS605 had been shown in other species to generate deletions adjacent to their sites of insertion (14,25,29). In two cases at least (IS1 and IS50) (25,32), deletion is independent of recA function, and we propose that an equivalent IS element-mediated adjacent-deletion process may have operated here.…”

Section: Discussionmentioning

confidence: 63%

Insertion of Mini-IS 605 and Deletion of Adjacent Sequences in the Nitroreductase ( rdxA ) Gene Cause Metronidazole Resistance in Helicobacter pylori NCTC11637

Debets-Ossenkopp

Pot

Westerloo

et al. 1999

Antimicrob Agents Chemother

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We found that NCTC11637, the type strain of Helicobacter pylori, the causative agent of peptic ulcer disease and an early risk factor for gastric cancer, is metronidazole resistant. DNA transformation, PCR-based restriction analysis, and DNA sequencing collectively showed that the metronidazole resistance of this strain was due to mutation in rdxA (gene HP0954 in the full genome sequence of H. pylori 26695) and that resistance did not depend on mutation in any of the other genes that had previously been suggested: catalase (katA), ferredoxin (fdx), flavodoxin (fldA), pyruvate:flavodoxin oxidoreductase (porγδαβ), RecA (recA), or superoxide dismutase (sodB). This is in accord with another recent study that attributed metronidazole resistance to point mutations inrdxA. However, the mechanism of rdxAinactivation that we found in NCTC11637 is itself also novel: insertion of mini-IS605, one of the endogenous transposable elements of H. pylori, and deletion of adjacent DNA sequences including 462 bp of the 851-bp-long rdxA gene.

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Section: Discussionmentioning

confidence: 63%

Insertion of Mini-IS 605 and Deletion of Adjacent Sequences in the Nitroreductase ( rdxA ) Gene Cause Metronidazole Resistance in Helicobacter pylori NCTC11637

Debets-Ossenkopp

Pot

Westerloo

et al. 1999

Antimicrob Agents Chemother

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“…Insertion sequences are small, autonomous, mobile genetic elements that encode a transposase and include accessory genes enclosed by terminal repeat sequences (20). Insertion sequences are widely recognized as drivers of bacterial evolution; they are often present in large numbers and serve as sites for homologous recombination and therefore chromosomal rearrangements, plasmid integration, and deletions (21). As composite transposons, they construct and disseminate novel metabolic pathways, including those involved in the catabolic degradation of substituted aromatics and xenobiotics (22, 23).…”

Section: Introductionmentioning

confidence: 99%

Structure and Evolution of Chlorate Reduction Composite Transposons

Clark

Melnyk

Engelbrektson

et al. 2013

mBio

114

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The genes for chlorate reduction in six bacterial strains were analyzed in order to gain insight into the metabolism. A newly isolated chlorate-reducing bacterium (Shewanella algae ACDC) and three previously isolated strains (Ideonella dechloratans, Pseudomonas sp. strain PK, and Dechloromarinus chlorophilus NSS) were genome sequenced and compared to published sequences (Alicycliphilus denitrificans BC plasmid pALIDE01 and Pseudomonas chloritidismutans AW-1). De novo assembly of genomes failed to join regions adjacent to genes involved in chlorate reduction, suggesting the presence of repeat regions. Using a bioinformatics approach and finishing PCRs to connect fragmented contigs, we discovered that chlorate reduction genes are flanked by insertion sequences, forming composite transposons in all four newly sequenced strains. These insertion sequences delineate regions with the potential to move horizontally and define a set of genes that may be important for chlorate reduction. In addition to core metabolic components, we have highlighted several such genes through comparative analysis and visualization. Phylogenetic analysis places chlorate reductase within a functionally diverse clade of type II dimethyl sulfoxide (DMSO) reductases, part of a larger family of enzymes with reactivity toward chlorate. Nucleotide-level forensics of regions surrounding chlorite dismutase (cld), as well as its phylogenetic clustering in a betaproteobacterial Cld clade, indicate that cld has been mobilized at least once from a perchlorate reducer to build chlorate respiration.

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“…(ii) Because the deletions involving w are fixed, endpoint deletions comparable to those generated in IS 1 in E. coli (8) and those involving y are bidirectional, a feature of IS4-generated deletions in E. coli (9), it seems reasonable to conclude that two distinctive IS are also involved in D. melanogaster.…”

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confidence: 99%

Genetic instability in Drosophila melanogaster: deletion induction by insertion sequences.

Green¹

1982

Proc. Natl. Acad. Sci. U.S.A.

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Females of Drosophila melanogaster heteroallelic or homoallelic for X chromosome giant (gt) mutants generate deletions involving the wild-type alleles at two X chromosome gene loci: yellow body color (y) and white eye color (w). The deletions, bidirectional in the case of y and with fixed endpoint in the case of w, are associated with particular X chromosomes. Distinctive insertion sequences, located proximal to the target loci, are presumed to generate the deletions.

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Bidirectional deletions associated with IS4

Cited by 10 publications

References 31 publications

Insertion of Mini-IS 605 and Deletion of Adjacent Sequences in the Nitroreductase ( rdxA ) Gene Cause Metronidazole Resistance in Helicobacter pylori NCTC11637

Insertion of Mini-IS 605 and Deletion of Adjacent Sequences in the Nitroreductase ( rdxA ) Gene Cause Metronidazole Resistance in Helicobacter pylori NCTC11637

Structure and Evolution of Chlorate Reduction Composite Transposons

Genetic instability in Drosophila melanogaster: deletion induction by insertion sequences.

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