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Chapter 16 : Transposition of

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Abstract:

This chapter is centered on studies of IS911 as a model system for studying the large IS3 group. The present understanding of the steps in IS911 transposition is shown. However, important insights and some intriguing differences have been revealed from other members and these are described where appropriate. Different roles for OrfA have been proposed for different IS3 family members: stimulation of transposon circle integration for IS911; inhibition of transposition for IS3; and repression of transposase expression for IS2. Mutation of the terminal dinucleotide at one or both ends of the junction significantly reduces cleavage of the mutated end in vivo and in vitro, and the same single- and double-end mutations strongly reduce the transposition frequency in vivo. In conclusion, by IS2, IS3, IS150, and IS911 probably share the same transposition pathway but may be differently regulated by OrfA and possibly by OrfB. Many transposable elements are separated from their flanking donor DNA prior to insertion into a target site. This behavior, termed cut-and-paste, requires processing of both strands at each end of the element.

Citation: Rousseau P, Normand C, Loot C, Turlan C, Alazard R, Duval-Valentin G, Chandler M. 2002. Transposition of , p 367-383. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch16

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Figures

Image of Figure 1
Figure 1

Organization of IS911. A cartoon of the IS is presented at the top of the figure. This includes the overlapping reading frames orfA and orfB (black boxes) together with their relative reading phases (0 and −1). The point of translational frameshifting is shown as a dotted vertical line. The 36 bp left and right terminal inverted repeats are shown as a heavy gray box and triangle, respectively. The endogenous promoter pIRL is also indicated. The RNA sequence encompassing the frameshift window is shown below. The potential orfB ribosome binding site is boxed, as is its AUU initiation codon. The ribosome engages the A6G slippery codons and slips one nucleotide to the left, as shown by the arrow. The structured downstream region is shown to the right and the orfA termination codon is indicated. The bottom of the figure shows the organization of IS911 proteins together with their molecular mass. The α helix-turn-α helix motif (HTH) is shown as a black square. Individual heptads of the leucine zipper (LZ) are represented by four ellipses. The unfilled ellipse shown in OrfA represents the heptad, which differs between OrfA and OrfAB. The catalytic domain is shown as a gray box including the DDE signature (black upright lines).

Citation: Rousseau P, Normand C, Loot C, Turlan C, Alazard R, Duval-Valentin G, Chandler M. 2002. Transposition of , p 367-383. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch16
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Image of Figure 2
Figure 2

Steps in the overall IS911 transposition pathway. The center shows a global view of the transposition process. The transposon is shown in bold, donor backbone sequences as fine lines, and target DNA as dotted lines. The small filled and unfilled circles represent IRL or IRR. The panels on the right of the figure show a finer view of the various steps. They illustrate (descending): cleavage at the terminal 5′CA3′ to generate a 3′OH and attack 3 bases (NNN) 5′ of the opposite (target) end. The junction of the figure eight with a free 3′OH in the vector strand is indicated (half arrow), together with the IRR-IRL circle junction and the associated promoter pjunc with −35 and −10 regions (unfilled boxes), the position of nucleophilic attack on both strands of the junction (arrows), target attack by the two liberated 3′OH groups on either side of the prospective 3-bp flanking target repeat (arrows), and the final insertion product ready to undergo repair.

Citation: Rousseau P, Normand C, Loot C, Turlan C, Alazard R, Duval-Valentin G, Chandler M. 2002. Transposition of , p 367-383. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch16
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Image of Figure 3
Figure 3

Predicted secondary structures. The map presents predicted β strands (filled boxes) and α helices (unfilled boxes). These are numbered b1 to b5 and h1 to h5, respectively, in order of those found in the crystal structure of the catalytic domain of HIV and ASV integrases. The positions of the mutations referred to in the text are indicated above. The relative positions of the different domains of the protein are boxed and indicated below.

Citation: Rousseau P, Normand C, Loot C, Turlan C, Alazard R, Duval-Valentin G, Chandler M. 2002. Transposition of , p 367-383. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch16
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Image of Figure 4
Figure 4

Synaptic complex A or paired-end complex. The scheme represents a model for complexes between the terminal inverted repeats and the truncated OrfAB derivatives. IRR is shown as a heavy black line with the terminal CA base pair labeled. The unfilled box shows the extent of protection by OrfAB[1–149] against DNase I attack in each isolated complex. Note that protection extends beyond the internal boundary of the IR. Complex I is shown as two paired ends retained by an unknown number of OrfAB[1–149] monomers. Complex II derives from complex I by titration of the DNA with high concentrations of protein. Complex III is shown to be generated by mixing a derivative with an M region (OrfAB[1–135], OrfAB[1–149]), and one without (OrfA, OrfAB[1–109]). The resulting uniquely bound OrfAB[1–135] or OrfAB[1–149] is shown either to change stoichiometry or configuration.

Citation: Rousseau P, Normand C, Loot C, Turlan C, Alazard R, Duval-Valentin G, Chandler M. 2002. Transposition of , p 367-383. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch16
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Image of Figure 5
Figure 5

Conversion of the figure-eight form to a circle and junction promoter assembly. (A) Resolution of the figure-eight form into a transposon circle may occur by resolution and repair (top pathway) or replication (bottom pathway). Transposon DNA is indicated in bold, donor backbone DNA by a thin line, and newly replicated DNA by a dotted line. Second-strand cleavage (top) would yield a gapped open circular form of the transposon, which could subsequently be repaired. The fate of the donor plasmid backbone is not determined. The pathway represented in the lower panels invokes replication using the 3′OH group (half arrow) located on the vector backbone at the junction with the transposon as a primer. (B) Schematic representation of the junction region. The proposed − 35 and − 10 regions are boxed, and the corresponding nucleotides are indicated in large script. The TGN sequence, also important in promoter activity (in this case TGG), is shown in italics. Those indicated below show pjunc while those above are pIRL. The nucleotides G, in bold and marked + 1, locate the transcriptional start for pjunc at nucleotide 22 and for pIRL at 56. The relative positions of IRR and IRL are also shown. Nucleotide coordinates are shown above the sequence initiating at the terminal T of IRL.

Citation: Rousseau P, Normand C, Loot C, Turlan C, Alazard R, Duval-Valentin G, Chandler M. 2002. Transposition of , p 367-383. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch16
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Image of Figure 6
Figure 6

[IS]2 formation from plasmid dimers, targeted insertion, and excision. (A) [IS]2 formation from plasmid dimers. A plasmid dimer is presented on the left. The transposon containing an orfA-lacZ translational fusion is shown as a crosshatched box. Open square and pointed boxes indicate the left and right terminal inverted repeats of IS911. The resident promoter, pIRL, partially located in IRL, is also shown. The open oval represents the plasmid origin of replication. Activation of the orfA-lacZ fusion by formation of an adjacent pjunc is indicated by the gray boxes. Reaction with OrfAB in vitro generates an inter-IS figure-eight form (center), which is converted into a form carrying a tandem IS dimer ([IS]2) following transformation into a suitable recA host strain. The IRR-IRL junction formed in this way carries the strong pjunc promoter, which drives expression of the orfA-lacZ translational fusion. (B) Targeted excision. The donor plasmid carries copies of IRR (pointed box) and IRL (square box) in the configuration of an active junction (IRR-IRL) with an additional appropriately oriented IRR. The transposon is indicated by a cross-hatched box. (C) Targeted insertion. Atransposon circle carrying a chloramphenicol resistance gene (Cm) is shown, together with a target plasmid carrying an inactivated transposon including an orfA-lacZ fusion (cross-hatched box). The small black circles on IRR and IRL indicate the presence of a mutation of the terminal CA dinucleotide. Activation of the orfA-lacZ fusion by insertion with formation of the junction promoter is indicated by a gray box.

Citation: Rousseau P, Normand C, Loot C, Turlan C, Alazard R, Duval-Valentin G, Chandler M. 2002. Transposition of , p 367-383. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch16
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Image of Figure 7
Figure 7

Recombination pathways in IS911 transposition. Transposon DNA is indicated by bold lines, donor plasmid DNA is indicated by thin lines, and target DNA is indicated by dotted lines. Left and right transposon ends are arbitrarily indicated by small filled and open circles. Half-arrows within the figure-eight forms indicate 3′OH ends, which may act as replication primers in the formation of circular forms from the figure-eight intermediates. The left part of the figure represents a monomeric plasmid generating a simple figure-eight form, which evolves into an IS circle and then undergoes simple insertion into a target DNA molecule. The central part of the figure shows a plasmid dimer, which undergoes intra-IS recombination to generate a figure-eight molecule, which then evolves into an IS circle and likewise undergoes simple insertion. The right part of the figure shows the same dimeric plasmid undergoing inter-IS recombination and evolution of the corresponding figure-eight molecule into a plasmid carrying a tandem IS dimer. Integration of this structure results in the formation of a cointegrate. A second pathway between IS dimers and IS monomeric circles is shown, which involves targeted integration into a monomeric plasmid to generate the [IS]2 copy and excision from the [IS]2 to generate the IS circle and a plasmid monomer.

Citation: Rousseau P, Normand C, Loot C, Turlan C, Alazard R, Duval-Valentin G, Chandler M. 2002. Transposition of , p 367-383. In Craig N, Craigie R, Gellert M, Lambowitz A (ed), Mobile DNA II. ASM Press, Washington, DC. doi: 10.1128/9781555817954.ch16
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