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本课件为《分子生物学》第15章转座子（Transposons），依据 Gene VII 教材编排，沿Insertion sequences、Composite等小节推进，讲解本章核心概念与分子机制，配逐页图示与文字版。
Chapter 15 Transposons
Transposon is a DNA sequence able to insert itself at a new location in the genome (without any sequence relationship with the target locus).
Transposon is a DNA sequence able to insert itself at a new location in the genome (without any sequence relationship with the target locus).
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ISis an abbrevi at ion for insertion sequence Transposase is the enzyme activity involved in insertion of transposon at a new site.
Figure 15.1 Transposons have inverted terminal repeats and generate direct repeats of flanking DNA at the target site. In this example, the target is a 5 bp sequence. The ends of the transposon consist of inverted repeats of 9 bp, where the numbers 1 through 9 indicate a sequence of base pairs.
Figure 15.2 A composite transposon has a central region carrying markers (such as drug resistance) flanked by IS modules. The modules have short inverted terminal repeats. If the modules themselves are in inverted orientation(as drawn), the short inverted terminal repeats at the ends of the transposon are identical.
Figure 15.3 Two IS10 modules create a composite transposon that can mobilize any region of DNA that lies between them. When Tn10 is part of a small circular molecule, the IS10 repeats can transpose either side of the circle.
Figure 15.4 The direct repeats of target DNA flanking a transposon are generated by the introduction of staggered cuts whose protruding ends are linked to the transposon.
Figure 15.5 Replicative transposition creates a copy of the transposon, which inserts at a recipient site. The donor site remains unchanged, so both donor and recipient have a copy of the transposon.
Figure 15.6 Nonreplicative transposition allows a transposon to move as a physical entity from a donor to a recipient site. This leaves a break at the donor site, which is lethal unless it can be repaired.
Figure 15.7 Conservative transposition involves direct movement with no loss of nucleotide bonds; compare with lambda integr at ion and excision.
Deletions are generated by removal of a sequence of DNA, the regions on either side being joined together.
Figure 15.8 Reciprocal recombination between direct repeats excises the material between them; each product of recombination has one copy of the direct repeat.
Figure 15.9 Reciprocal recombination between inverted repeats inverts the region between them.
Figure 15.10 Transposition is initiated by nicking the transposon ends and target site and joining the nicked ends into a strand transfer complex.
Figure 15.11 Mu transposition passes through three stable stages. MuA transposase forms a tetramer that synapses the ends of phage Mu. Transposase subunits act in transto nick each end of the DNA; then a second trans action joins the nicked ends to the target DNA.
Resolvase is enzyme activity involved in site-specific recombination between two transposons present as direct repeats in a cointegrate structure.
Figure 15.12 Transposition may fuse a donor and recipient replicon into a cointegrate. Resolution releases two replicons, each containing a copy of the transposon.
Figure 15.13 Mu transposition generates a crossover structure, which is converted by replication into a cointegrate.
Figure 15.14 Nonreplicative transposition results when a crossover structure is released by nicking. This inserts the transposon into the target DNA, flanked by the direct repeats of the target, and the donor is left with a double-strand break.
Figure 15.6 Nonreplicative transposition allows a transposon to move as a physical entity from a donor to a recipient site. This leaves a break at the donor site, which is lethal unless it can be repaired.
Figure 15.15 Both strands of Tn10 are cleaved sequentially, and then the transposon is joined to the nicked target site.
Figure 15.13 Mu transposition generates a crossover structure, which is converted by replication into a cointegrate.
Figure 15.16 Cleavage of Tn5 from flanking DNA involves nicking, interstr and reaction, and hairpin cleavage.
Figure 15.17 Each subunit of the Tn5 transposase has one end of the transposon located in its active site and also makes contact at a different site with the other end of the transposon.
Figure 15.18 Transposons of the TnA family have inverted terminal repeats, an internal ressite, and three known genes.
Figure 15.18 Transposons of the TnA family have inverted terminal repeats, an internal ressite, and three known genes.
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Figure 15.19 Two promoters in opposite orientation lie near the out side boundary of IS10R. The strong promoter POUT sponsors transcription toward the flanking host DNA. The weaker promoter PIN causes transcription of an RNA that extends the length of IS10R and is translated into the transposase.
Figure 15.20 Several mechanisms restrain the frequency of Tn10 transposition, by affecting either the synthesis or function of transposase protein. Transposition of an individual transposon is restricted by methylation to occur only after replication. In multicopy situ at ions, cis-preference restricts the choice of target, and OUT/IN RNA pairing inhibits synthesis of transposase.
Figure 15.6 Nonreplicative transposition allows a transposon to move as a physical entity from a donor to a recipient site. This leaves a break at the donor site, which is lethal unless it can be repaired.
Acentric fragmentof a chromosome (generated by breakage) lacks a centromere and is lost at cell division.
Figure 15.21 Clonal analysis identifies a group of cells descended from a single ancestor in which a transposition-mediated event altered the phenotype. Timing of the event during development is indicated by the number of cells; tissue specificity of the event may be indicated by the location of the cells.
Figure 15.22 A break at a controlling element causes loss of an acentric fragment; if the fragment carries the dominant markers of a heterozygote, its loss changes the phenotype. The effects of the dominant markers, CI, Bz, Wx, can be visualized by the color of the cells or by appropriate staining.
Figure 15.23 Ds provides a site to initiate the chromatid fusion-bridge-breakage cycle. The products can be followed by clonal analysis.
Figure 15.24 Each controlling element family has both autonomous and nonautonomous members. Autonomous elements are cap able of transposition. Nonautonomous elements are deficient in transposition. Pairs of autonomous and nonautonomous elements can be classified in >4 families.
Figure 15.25 The Ac element has two open reading frames; Ds elements have internal deletions.
Figure 15.22 A break at a controlling element causes loss of an acentric fragment; if the fragment carries the dominant markers of a heterozygote, its loss changes the phenotype. The effects of the dominant markers, CI, Bz, Wx, can be visualized by the color of the cells or by appropriate staining.
Figure 15.26 Spm/En has two genes. tnpA consists of 11 exons that are transcribed into a spliced 2500 base mRNA. tnpB may consist of a 6000 base mRNA containing ORF1 + ORF2.
Hybrid dysgenesis describes the inability of certain strains of D. melanogaster to interbreed, because the hybrids are sterile (although otherwise they may be phenotypically normal).
Figure 15.27 Hybrid dysgenesis is asymmetrical; it is induced by P male xM female crosses, but not by M male xP female crosses.
Figure 15.28 The P element has four exons. The first three are spliced together in somatic expression; all four are spliced together in germline expression.
Figure 15.6 Nonreplicative transposition allows a transposon to move as a physical entity from a donor to a recipient site. This leaves a break at the donor site, which is lethal unless it can be repaired.
Figure 15.29 Hybrid dysgenesis is determined by the interactions between P elements in the genome and 66 kD repressor in the cytotype.
Summary
Summary
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