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Chapter 19 : Tn7

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Abstract:

The bacterial transposon Tn is a sophisticated mobile element that pursues several alternative lifestyles to promote its propagation. Tn was first isolated from a trimethoprim- and streptomycin-resistant bacterium in a calf that was being treated prophylactically with trimethoprim in its feed. The genes are all oriented in the same direction with their 5' ends toward the right end of Tn. These genes were identified genetically by analysis of deletion and insertion derivatives of Tn and by gene sequencing, protein identification, and protein purification (TnsA, TnsB, TnsC, TnsD, and TnsE). The topological requirements of the donor DNA substrate have been examined in the in vitro Tn transposition system. The partial sequence of another TnsA gene distinct from the others has also been described, suggesting that more close relatives of Tn remain to be discovered. Transposons have long been useful tools for the manipulation of genes and genomes. The study of Tn has enriched the study of mobile DNA; there are distinct differences between Tn and other elements as well as similarities between Tn and other elements. The study of Tn seems sure to continue to provide an interesting system in which to examine the interaction of a transposable element with its host, to provide interesting problems in protein-DNA and protein-protein interactions to study, and to provide useful tools for the study and manipulation of genes and genomes.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19

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Figures

Image of Figure 1
Figure 1

Tntransposition is modulated by different aspects of target DNAs. Tnis preferentially attracted to a single specific site in the chromosomes of many bacteria, a lifestyle that promotes vertical transmission of the element. Tnis also preferentially attracted to conjugating plasmids, likely because of the unique form of lagging-strand synthesis that occurs upon mating. These different targeting pathways are mediated by different subsets of Tn-encoded transposition proteins. Preferential insertion on conjugating plasmids provides a lifestyle that promotes dispersal of Tnbetween organisms. Tnavoids DNA containing Tnthereby avoiding self-destruction.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 2
Figure 2

Tntranslocates via cut-and-paste transposition. The substrate DNAs are a donor DNA containing Tnand a target plasmid containing Recombination initiates by double-strand breaks at either end of the Tnelement; a second break generates an excised transposon species that is then inserted into The other product of the reaction is a gapped donor backbone plasmid.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 3
Figure 3

Map of TnThe transposition genes (and ) are all carried in the right end of Tnwith their 5′ termini closest to the right terminus of TnThe left end of Tncarries several antibiotic resistance genes: which provides resistance to trimethoprim; which provides resistance to streptothricin; and which provides resistance to streptomycin and spectinomycin. These antibiotic resistance cassettes are part of an integron element

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 4
Figure 4

The ends of TnThe Tn7L and Tn7R end segments contain multiple copies of the 22-bp TnsB binding sequence as defined by TnsB-footprinting studies. The 30-bp nearly perfect inverted repeats contain a perfect 8-bp terminal inverted repeat (bold) containing a critical 5′-TGT . . . .ACA-3′, a 5-bp spacer region and a TnsB binding site.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 5
Figure 5

Tninsertion into The specific point of Tninsertion lies between and Tninserts into in a specific orientation with the right end of Tnadjacent to The position designated 0 is the center of the target 5 bp duplicated upon Tninsertion, base pairs rightward toward are designated  and base pairs leftward are designated –.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 6
Figure 6

Tntransposition chemistry. In the donor site, Tnis flanked by a 5-bp duplication of target sequences resulting from the insertion of Tninto that site. Tnis excised from the donor site by double-strand breaks. Cleavage at the transposon ends is staggered: cleavage occurs precisely at the 3′ ends of the element but occurs within the flanking donor DNA such that 3 nucleotides of flanking donor sequences (indicated by “d”) are attached to the 5′ ends of the transposon. The 3′ ends of the transposon attack staggered positions on the target DNA (indicated by “t”), generating a new insertion flanked by short gaps. The donor nucleotides on the 5′ ends of the transposon are removed and the gaps are repaired by host functions.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 7
Figure 7

The processing events at the ends of Tnare mediated by two different polypeptides. TnsB mediates the cleavages at the 3′ ends of Tnand the joining of the exposed 3′-OHs to the target DNA. TnsA mediates the cleavages at the 5′ ends of TnTransposase activity requires TnsA and TnsB: no activity is seen in the presence of either protein alone.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 8
Figure 8

Double-strand breaks at transposon ends can occur by multiple mechanisms. Whereas Tnuses cleavages by two different polypeptides to generate double-strand breaks at the ends of TnISand ISuse a one polypeptide and a hairpinning mechanism to generate double-strand breaks. With ISand ISa nick is introduced at the 3′ end of the transposon. The resulting 3′-OH intramolecularly attacks the 5′ strand of the transposon to form a hairpin on the transposon end; this step also disconnects the transposon from the flanking donor DNA. The transposase then opens the hairpin, again exposing the 3′ end of the transposon which can go on to attack the target DNA.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 9
Figure 9

The gapped donor site can be repaired. The gapped donor site that results from transposon excision can be repaired by double-strand break repair using another copy of the donor site. Such repair can be visualized by examination of cells containing heteroalleles: one ::Tnallele and the other a heteroallele mutant at a site that does not overlap the Tninsertion site. When Tntransposition occurs, that is, Tnexcises from the ::Tn7 site, the resulting gap can use information in the heteroallele to convert the gapped region of the Tndonor site to .

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 10
Figure 10

Cut-and-paste transposition can be biologically replicative. The large square is a bacterial cell with two copies of the bacterial chromosome, each containing a transposable element. Transposition of the transposon from one DNA into the other results in one gapped chromosome and one chromosome containing two copies of the element, one at the donor site and one at the new site of insertion. Thus, when cells containing the bacterial chromosome with the two copies of the element are examined, transposition looks replicative, although the element actually moved by cut-and-paste transposition.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 11
Figure 11

Tntransposition can switch from a cut-and-paste mechanism to a replicative mechanism. The cut-and-paste pathway in which Tnexcises from the donor site is shown on the left. On the right in the replicative pathway, nicks occur at the 3′ ends of the transposon. These 3′ ends then attack the target DNA to form the fusion product in which the transposon links the donor and target DNAs. Repair and replication of this fusion product yield the cointegrate that contains two copies of the mobile element.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 12
Figure 12

Products of intramolecular Tntransposition. The upper line shows a linearized Tn-containing plasmid DNA before recombination. Recombination initiates by a double-strand break at either the left end (DSB.L) or right end (DSB.R) of TnThe 3′-OH ends exposed by these double-strand breaks then attack the 5′ strands at the other ends of the transposon, generating species called ;“single end joins” (SEJ) that contain circularized versions of Tn

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 13
Figure 13

Tn“;figures of eight.” The upper line shows a linearized Tn-containing plasmid DNA before recombination. When recombination occurs with TnsATnsB, where TnsA is blocked for cleavage at the 5′ ends of Tnonly single-strand cleavage occurs at either the left or right 3′ end of TnThese exposed 3′ ends then execute an intramolecular attack at the 5′ strand at the other end of the transposon, generating figures of eight.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 14
Figure 14

Structures of TnsB and TnsA. (A) TnsB and TnsA are indicated as open bars. The DNA binding domain of TnsB (1 to 241) that specifically recognizes the ends of Tnis indicated by a cross-hatched bar. The catalytic amino acids D273, D361, and E396 are indicated in TnsB and E63, D114, Q130, K132, and E149 in TnsA (gray bars). Gain-of-function mutations in TnsA and TnsB that allow recombination under the indicated conditions are shown. (B) Alignment of TnsB with other members of the Retroviral Integrase Superfamily. This alignment of the catalytic domains of these recombinases was generated by the Conserved Domain Database at the National Center for Biotechnology Information. The acidic amino acids in bold are the DDE motif. (C) Gain-of-function mutations in TnsA that allow recombination in the presence of TnsATnsBTnsC lie on the back of the helix containing the TnsA active-site amino acids E63. Reprinted from reference with permission

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 15
Figure 15

TnsC bound to the target DNA provides a platform for the transposase. The TnsAB transposase bound to the ends of Tnis positioned on the target DNA through the interaction with TnsC. The interaction of TnsC with the transposase activates the breakage and joining events that underlie transposition. The boundaries of TnsC interaction with the target DNA are those observed in TnsCTnsD-The transposase attacks the target site at 5′-staggered positions on the target DNA.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 16
Figure 16

Modulation of TnsC activity. TnsC stimulates the transposase to execute breakage and joining when bound to ATP and the target DNA. The presence of particular targeting proteins and target DNAs determines the ATP and DNA state of TnsC.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 17
Figure 17

. Positions of gain-of-function mutations in TnsC that allow recombination with TnsA +TnsB+TnsC. The TnsC polypeptide is indicated by the open bar; the positions of the Walker A and B motifs for purine nucleotide utilization are indicated by hatched bars. Class I gain-of-function mutations remain sensitive to target DNA signals; they are sensitive to transposition immunity and are directed to appropriate target sites by TnsD and TnsE. Class II mutants are insensitive to target signals; they promote transposition into immune targets and do not respond to TnsD and TnsE. Reprinted from reference with permission.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 18
Figure 18

Comparison of patterns of insertions promoted by TnsABC into duplex- and triplex-containing DNA targets. (A) Transposition was performed in vitro using a duplex DNA. The transposition products were recovered by transformation into and the sequences of 100 products determined. The filled circles represent insertions in one orientation with respect to the target backbone and the open circles in the other. The hatched region is the origin-of-replication region. (B) Transposition was performed in vitro into a triplex DNA target formed by annealing a triplex-forming oligonucleotide to the plasmid and psoralen cross-linking. Insertions were recovered and mapped as described above.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 19
Figure 19

Tninsertion into Tninserts about 25 bp to the 5′ side of the TnsD binding site. The TnsD binding site lies in the C-terminal region of the gene and the actual point of Tninsertion lies in the transcription terminator. The middle of the 5 bp duplicated upon Tninsertion is designated 0; sequences to the right are indicated by plus signs, and sequences to the left are indicated by a minus sign.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 20
Figure 20

Positions of Tns protein binding on The positions of TnsD and TnsC-TnsD binding on as evaluated by various footprinting methods are shown. The position of a TnsD-induced distortion in DNA at +27 is also indicated. Deletion of this region of distortion decreases TnsD and TnsCD binding to and target activity.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 21
Figure 21

Target DNA structure plays a key role in Tninsertion. Similar features of the target DNA and Tninsertion during insertion into and adjacent to triplex DNA emphasize the critical role of target DNA structure. Target DNA distortions indicated by cross-hatching in and at triplex DNA have been detected by DNA footprinting. Reprinted from reference with permission.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 22
Figure 22

A model for Tninsertion at The binding of TnsD to results in the formation of a TnsC-TnsD-complex. The binding of TnsD results in a DNA distortion (shaded bar at +27) which attracts TnsC. TnsC that is bound in the minor groove provides a platform for the interaction and activation of the TnsAB transposase that is bound on the transposon ends. The transposase and transposon ends must attack the target DNA across the major groove.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 23
Figure 23

Orientation of TnsABC+E insertions in the chromosome. The position of the origin of replication () and the sites (triangles) are marked as the two chromosomal replicores (dashed lines). The positions of 50 TnsABC+E insertions (arrows) promoted by TnsE mutants that are more active than wild-type TnsE are also marked; those outside the chromosomal circle lie in one orientation with respect to the chromosome, whereas those inside are inserted in the opposite orientation. Reprinted from reference with permission.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 24
Figure 24

Disposition of TnsABC+E insertions with respect to lagging-strand DNA synthesis in various replicons. (A) Tninsertion into conjugating plasmids occurs in a single orientation in recipient cells, independent of the insertion position within the plasmid. Insertion occurs in the orientation indicated with respect to lagging-strand DNA synthesis in the recipient. (B) Tninsertions occur in different orientations in each of the chromosomal replicores as indicated; in both replicores, insertion occurs in the same orientation with respect to lagging-strand DNA synthesis

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 25
Figure 25

Positions of TnsABC+E insertions in the chromosome. (A) A physical map of the chromosome based on digestion with certain rare cutting restriction enzymes is shown. The positions of the origin of DNA replication () and several of the possible termination sites (to ) are shown. (B) The distribution of 35 TnsABC+E insertions per 100 kb within the chromosome. The error bar represents the change in insertion frequency with one more or one less insertion in that region. (C) The distribution of 34 TnsABC-mediated insertions that occur in the absence of TnsE.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 26
Figure 26

The distribution of TnTnsABC+E insertions in a chromosome containing a double-strand break. A double-strand break was introduced into the bacterial chromosome by Tnexcision and the positions of Tninsertions determined. Reprinted from reference with permission.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 27
Figure 27

Transposition immunity in the chromosome. The mean fraction of Tninsertion from F::Tn7 into in chromosomes containing immobile mini-Tnends at different distances from is expressed relative to Tninsertion into chromosomes without a mini-Tnelement (100% = 2.3% Tnoccupancy) as assayed by Southern blotting. The contribution of background hybridization to the Tninsertion signal in cells without a mini-Tnelement was determined from assays of cells lacking Tnand is displayed as a dashed line. Reprinted from reference with permission.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Image of Figure 28
Figure 28

A model for Tntransposition immunity. Tninsertion into a target molecule results from the interaction of the TnsAB transposase bound to the Tnelement with TnsC on an appropriate target DNA (or TnsCD-or TnsCE-target DNA). A target DNA containing a Tnend is immune to Tninsertion because TnsB interacts with that end and with TnsC to result in the removal of TnsC from the target DNA. Reprinted from reference with permission.

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19
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Tables

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Table 1

Transposons with ATP-utilizing proteins

Citation: Craig N. 2002. Tn7, p 423-456. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch19

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