1. Figure: 21-01
Title:
Transposons have inverted repeats and generate target repeats
Caption:
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.

2. Figure: UN
Title:
Caption:

3. Figure: UN
Title:
Caption:

4. Figure: 21-02
Title:
Tn9 has repeated IS modules
Caption:
The composite transposon Tn9 has a central region with a drug resistance marker, flanked by two copies of IS1 in the same orientation. Both copies of IS1 are functional.

5. Figure: 21-03
Title:
Tn10 has inverted IS modules
Caption:
Tn10 has a central region with a drug resistance marker, flanked by two copies of IS10 in opposite orientations. Only the IS10R copy is functional.

6. Figure: 21-04
Title:
Direct repeats are generated by insertion
Caption:
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.

7. Figure: 21-05
Title:
Transposon is copied to new site
Caption:
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.

8. Figure: 21-06
Title:
Transposon moves to new site
Caption:
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 repaired.

9. Figure: 21-07
Title:
Direct repeats recombine to excise material
Caption:
Reciprocal recombination between direct repeats excises the material between them; each product of recombination has one copy of the direct repeat.

10. Figure: 21-08
Title:
Inverted repeat recombination inverts material
Caption:
Reciprocal recombination between inverted repeats inverts the region between them.

11. Figure: 21-09
Title:
Transposition initiates by nicking ends
Caption:
Transposition is initiated by nicking the transposon ends and target site and joining the nicked ends into a strand transfer complex.

12. Figure: 21-10
Title:
Mu transposase catalyzes the reaction
Caption:
Mu transposition passes through three stable stages. MuA transposase forms a tetramer that synapses the ends of phage Mu. Transposase subunits act in trans to nick each end of the DNA; then a second trans action joins the nicked ends to the target DNA.

13. Figure: 21-11
Title:
Mu transposition uses a crossover intermediate
Caption:
Mu transposition generates a crossover structure, which is converted by replication into a cointegrate.

14. Figure: 21-12
Title:
Donor and recipient fuse into cointegrate
Caption:
Transposition may fuse a donor and recipient replicon into a cointegrate. Resolution releases two replicons, each containing a copy of the transposon.

15. Figure: 21-13
Title:
A crossover can be released by nicking
Caption:
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.

16. Figure: 21-14
Title:
Transposition can use cleavage and ligation
Caption:
Both strands of Tn10 are cleaved sequentially, and then the transposon is joined to the nicked target site.

17. Figure: 21-15
Title:
Tn5 is cleaved from flanking DNA
Caption:
Cleavage of Tn5 from flanking DNA involves nicking, interstrand reaction, and hairpin cleavage.

18. Figure: 21-16
Title:
Transposon ends are joined
Caption:
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.

19. Figure: 21-17
Title:
TnA transposon organization is conserved
Caption:
Transposons of the TnA family have inverted terminal repeats, an internal res site, and three known genes.

20. Figure: UN
Title:
Caption:

21. Figure: 21-18
Title:
Transpositional are clonally inherited
Caption:
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.

22. Figure: 21-19
Title:
Acentric fragments are lost
Caption:
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.

23. Figure: 21-20
Title:
Ds causes a breakage-fusion-bridge cycle
Caption:
Ds provides a site to initiate the chromatid breakage-fusion-bridge cycle. The products can be followed by clonal analysis.

24. Figure: 21-21
Title:
Transposons are autonomous or nonautonomous
Caption:
Each controlling element family has both autonomous and nonautonomous members. Autonomous elements are capable of transposition. Nonautonomous elements are deficient in transposition. Pairs of autonomous and nonautonomous elements can be classified in >4 families.

25. Figure: 21-22
Title:
Ds elements are deletions of Ac
Caption:
The Ac element has five exons that code for a transposase; Ds elements have internal deletions.

26. Figure: UN
Title:
Caption:

27. Figure: 21-23
Title:
P male  M female crosses are infertile
Caption:
Hybrid dysgenesis is asymmetrical; it is induced by P male  M female crosses, but not by M male  P female crosses.

28. Figure: 21-24
Title:
P element splicing is tissue-specific
Caption:
The P element has four exons. The first three are spliced together in somatic expression; all four are spliced together in germline expression.

29. Figure: 21-25
Title:
P elements are controlled by a repressor
Caption:
Hybrid dysgenesis is determined by the interactions between P elements in the genome and 66 kD repressor in the cytotype.

30. Figure:
Title:
P elements are controlled by a repressor
Caption:
Hybrid dysgenesis is determined by the interactions between P elements in the genome and 66 kD repressor in the cytotype.

31. Figure:
Title:
P elements are controlled by a repressor
Caption:
Hybrid dysgenesis is determined by the interactions between P elements in the genome and 66 kD repressor in the cytotype.

32. Figure:
Title:
P elements are controlled by a repressor
Caption:
Hybrid dysgenesis is determined by the interactions between P elements in the genome and 66 kD repressor in the cytotype.