Genetic Organization of Tn5

Rothstein, Steven J.; Jorgensen, Richard A.; Yin, Jie; Yong-di, Z.; Johnson, Russell D.; Reznikoff, W S

doi:10.1101/sqb.1981.045.01.018

Cited by 49 publications

(30 citation statements)

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“…Like other transposable elements, they encode an enzymatic activity, termed transposase, which catalyzes insertion of copies of the IS into novel chromosomal locations. The DNA sequences of several IS elements, including IS10 (102), IS50 (171), and IS903 (73), include a long ORF which was assumed to encode transposase. By contrast, the DNA sequences of a larger number of other elements show no sign of such a gene product.…”

Section: Programmed ؊1 Frameshift Sites In Bacteriamentioning

confidence: 99%

Programmed Translational Frameshifting

1996

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▪ Abstract Errors that alter the reading frame occur extremely rarely during translation, yet some genes have evolved sequences that efficiently induce frameshifting. These sequences, termed programmed frameshift sites, manipulate the translational apparatus to promote non-canonical decoding. Frameshifts are mechanistically diverse. Most cause a −1 shift of frames; the first such site was discovered in a metazoan retrovirus, but they are now known to be dispersed quite widely among evolutionarily diverse species. +1 frameshift sites are much less common, but again dispersed widely. The rarest form are the translational hop sites which program the ribosome to bypass a region of several dozen nucleotides. Each of these types of events are stimulated by distinct mechanisms. All of the events share a common phenomenology in which the programmed frameshift site causes the ribosome to pause during elongation so that the kinetically unfavorable alternative decoding event can occur. During this pause most frameshifts occur because one or more ribosome-bound tRNAs slip between cognate or near-cognate codons. However, even this generalization is not entirely consistent, since some frameshifts occur without slippage. Because of their similarity to rarer translational errors, programmed frameshift sites provide a tool with which to probe the mechanism of frame maintenance.

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Section: Programmed ؊1 Frameshift Sites In Bacteriamentioning

confidence: 99%

Programmed Translational Frameshifting

1996

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“…Plasmid pKPG10 contains the internal HindIII fragment from transposon 5 (Tn5) inserted at the HindIII site on pBR322 (9). The Tn5 fragment and pKPG10 do not carry a functional Tn5 transposase gene (16). Thus, the recombinations involving pKPG10 were not catalyzed by the Tn5 transposase (6).…”

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confidence: 99%

Role of short regions of homology in intermolecular illegitimate recombination events.

Marvo¹,

King²,

Jaskunas³

1983

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

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The structures of three recombinants between bacteriophage A DNA and plasmid pBR322 that were generated in a recA derivative of Escherichia coli are described. Each resulted from two illegitimate recombination events that resulted in the substitution of part of the A genome by part of the plasmid genome. The nucleotide sequences at the six A-plasmid junctions were determined and compared with the sequences of the A and plasmid genomes before recombination. Each recombination occurred at a short region of homology in the two genomes, and other short regions of homology were found near some of the junctions. The structures of these junctions are similar to those resulting from illegitimate recombination in animal cells. A model to explain how these multiple illegitimate recombination events could result from a cascade of DNA gyrase-catalyzed recombinations is discussed.The mechanisms responsible for generating gross DNA rearrangements such as deletions, substitutions, inversions, amplifications, and translocations are not understood. Recently, two specific models have been proposed that could account for these illegitimate recombination events.Miller and co-workers (1, 2) have found that most deletions in Escherichia coli occur between directly repeated sequences of 5 or more base pairs (bp). Therefore, they suggested that these deletions resulted from a slippage error in replication (2). Efstratiadis et al. (3) have suggested a similar model for the generation of deletions in eukaryotic cells.Another possible explanation for some illegitimate recombination events is that they are generated by DNA gyrase (4-6). Ikeda et aL (4, 5) discovered that illegitimate recombinations between A DNA and plasmid pBR322 occur in extracts of E. coli and that the frequency of recombination is increased by the addition of oxolinic acid (4, 5), which is an inhibitor of DNA gyrase (7,8). Therefore, they suggested that the recombinations result from an exchange of DNA gyrase subunits bound to different sites. The nucleotide sequences at the A-plasmid junctions of one of these recombinants were determined and the results were consistent with this model (5).We have isolated several A-pBR322 recombinants that were generated in recA+ and recA-derivatives of E. coli (6,9). The sequences at the A-pBR322 junctions of four of these recombinants were determined (6). Each resulted from reciprocal recombination between 10-13 bp of homology in A DNA and pBR322, including one (ATA1R) that was isolated in a recAstrain. One of the recombinants, AKA7, had an unusual structure in that it resulted from two of these rare events. DNA gyrase appears to be capable of catalyzing multiple recombinations (4). Therefore, we have suggested that AKA7 may have been generated by a cascade of DNA gyrase-catalyzed recombinations (6).The structures of three additional A-pBR322 recombinants isolated in a recA-strain of E. coli are described here. Each resulted from two recombinations at sites of 1-5 bp of homology in the A and plasmid genomes. Their structur...

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“…4). Tn.5 has been investigated with regard to expression of transposition functions and neomycin phosphotransferase (NPT) I1 activity and the promoters for these functions have been identified (Rothstein et al, 1980). However, it is not readily apparent from this information how read-through transcription could account for the different amidase activities in E. coli.…”

Section: Discussionmentioning

confidence: 99%

Complementation Analysis of the Aliphatic Amidase Genes of Pseudomonas aeruginosa

Drew

1984

Microbiology

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A plasmid, pCL34, capable of autonomous replication in Escherichia coli and Pseudomonas aeruginosa has been constructed which carries the promoter and structural gene (amiE) for P. aeruginosa amidase, but not the regulator gene (amiR). Plasmid pCL34 has been mobilized from E. coli to P. aeruginosa using the broad host range plasmid RP4. Complementation studies were performed in P. aeruginosa strains carrying various amidase mutations. Measurements of amidase activity in the recipients under inducing, non-inducing and repressing conditions showed trans-complementation by the chromosomally located regulator gene product. These results confirmed the positive control model for amidase gene expression. Levels of amidase expression seen during these studies were approximately threefold higher than in the parental, amidase-positive strains.

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Genetic Organization of Tn5

Cited by 49 publications

References 0 publications

Programmed Translational Frameshifting

Programmed Translational Frameshifting

Role of short regions of homology in intermolecular illegitimate recombination events.

Complementation Analysis of the Aliphatic Amidase Genes of Pseudomonas aeruginosa

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