DNA-only transposons can relocate from a donor site to a target site by cutand-paste transposition (Figure 5–61). Here, the transposon is literally excised from one spot on a genome and inserted into another. This reaction produces a short duplication of the target DNA sequence at the insertion site; these direct repeat sequences that flank the transposon serve as convenient records of prior transposition events. Such “signatures” often provide valuable clues in identifying transposons in genome sequences.
When a cut-and-paste DNA-only transposon is excised from its original location, it leaves behind a “hole” in the chromosome. This lesion can be perfectly healed by recombinational double-strand break repair (see Figure 5–48), provided that the chromosome has just been replicated and an identical copy of the damaged host sequence is available. Alternatively, a nonhomologous end-joining reaction can reseal the break; in this case, the DNA sequence that originally flanked the transposon is altered, producing a mutation at the chromosomal site from which the transposon was excised (see Figure 5–45).
Remarkably, the same mechanism used to excise cut-and-paste transposons from DNA has been found to operate in developing immune systems of short direct repeats of target DNA sequences in chromosome B
Figure 5–60 Three of the many DNA-only transposons found in bacteria. Each of these mobile DNA elements contains a gene that encodes a transposase, an enzyme that carries out the DNA breakage and joining reactions needed for the element to move. Each transposon also carries short DNA sequences (indicated in red) that are recognized only by the transposase encoded by that element and are necessary for movement of the element. In addition, two of the three mobile elements shown carry genes that encode enzymes that inactivate the antibiotics ampicillin (AmpR)—a penicillin derivative—and tetracycline (TetR). The transposable element Tn10, shown in the bottom diagram, is thought to have evolved from the chance landing of two much shorter mobile elements on either side of a tetracycline-resistance gene.
Figure 5–61 Cut-and-paste transposition. DNA-only transposons can be recognized in chromosomes by the “inverted repeat DNA sequences” (red) present at their ends. These sequences, which can be as short as 20 nucleotides, are all that is necessary for the DNA between them to be transposed by the particular transposase enzyme associated with the element. The cut-and-paste movement of a DNA-only transposable element from one chromosomal site to another begins when the transposase brings the two inverted DNA sequences together, forming a DNA loop. Insertion into the target chromosome, also catalyzed by the transposase, occurs at a random site through the creation of staggered breaks in the target chromosome (purple arrowheads). Following the transposition reaction, the single-strand gaps created by the staggered breaks are repaired by DNA polymerase and ligase (black). As a result, the insertion site is marked by a short direct repeat of the target DNA sequence, as shown. Although the break in the donor chromosome (green) is repaired, this process often alters the DNA sequence, causing a mutation at the original site of the excised transposable element (not shown).
vertebrates, catalyzing the DNA rearrangements that produce antibody and T cell receptor diversity. Known as V(D)J recombination, this process will be discussed in Chapter 24. Found only in vertebrates, V(D)J recombination is a relatively recent evolutionary novelty, but it is believed to be derived from the much more ancient cut-and-paste transposons.
Some Viruses Use a Transposition Mechanism to Move Themselves Into Host-Cell Chromosomes