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Chapter 25 : Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences

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Abstract:

Strand mispairing interactions between repeated DNA sequences provoke a host of mutations and genetic rearrangements in bacteria. Repeated DNA sequences in either direct or inverted orientation can promote misalignment-mediated mutations and rearrangements by very similar mechanisms. This chapter catalogs several types of misalignment-mediated genetic changes in bacteria, with an emphasis on the mechanisms by which they occur. Systematic study of misalignment-mediated mutation and genetic rearrangements has revealed many elements of the mechanisms of these processes, including the integral role for DNA replication. The impact of these misalignment processes on bacterial physiology and genomic evolution is also discussed in this chapter. Sister chromosome exchange (SCE)-associated misalignment has been studied only on plasmid replicons. When recA-independent deletions or expansions between tandem repeats are selected on plasmids, concomitant replicon dimerization is often seen. Single-strand annealing (SSA) contributes as a major pathway to rearrangements in eukaryotes and in bacteriophage-infected but may occur efficiently only under restricted circumstances in normal bacterial growth. Short spurious repeats can be sites for deletion, duplication, or inversion; these processes create larger repeats that can lead to even higher rates of rearrangements. These rearrangements can occur independently of the bacterial homologous recombination pathways and are dependent on the length and perfection of the repeats, as well as their proximity.

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25

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Figures

Image of Figure 1
Figure 1

Frameshifts by slipped misalignment. “Slippage” of the nascent strand with its template leading to -1 frameshift (A) or +1 frameshift (B) mutations is shown. The one base loop in the slippage intermediate is efficiently recognized by the mismatch repair (MMR) system, leading to excision of the nascent strand and removal of the potential frameshift.

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25
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Image of Figure 2
Figure 2

Dislocation mutagenesis by transient slipped misalignment. Transient slipped misalignment between imperfect or quasirepeats can cause a mutation to be templated. A second strand switch restores normal alignment, leaving a mismatched heteroduplex intermediate.

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25
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Image of Figure 3
Figure 3

Long-range slipped misalignment and tandem repeat deletion or expansion. Slipped misalignment can occur between direct repeats, leading to deletion of one repeat and any intervening material (A) or duplication of one repeat and the intervening sequence (B). The long-range slippage intermediate consists of a large single-stranded loop, which is not recognized by the mismatch repair system. However, if sequence heterologies exist between the two direct repeats, mismatches in the heteroduplex region of the slipped intermediate elicit mismatch repair.

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25
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Image of Figure 4
Figure 4

Gene amplification through tandem direct-repeat arrays. Short repeats in DNA (A) promote a gene duplication (B) through RecA-dependent recombination or RecA-independent slippage. Formation of the initial gene duplication is the rate-limiting step. Under selection for high gene expression, the duplication expands to higher copy, usually through RecA-dependent recombination at the large direct repeats (C). In the absence of selection, the amplicon collapses to a single-copy locus (D), again usually by RecA-dependent homologous recombination.

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25
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Image of Figure 5
Figure 5

Deletion associated with SCE by cross-fork slipped misalignment. In a blocked replication fork, slipped misalignment can occur between the nascent strands at direct repeat sequences (asterisk). After processing of the Holliday junction branched intermediate, crossovers between the sister chromosomes can occur concomitantly with a reciprocal rearrangement (formation of both deletion and triplication product). Such crossing-over can be recognized since it leads to replicon dimerization.

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25
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Image of Figure 6
Figure 6

Inverted repeat stimulation of deletion at direct repeats. Inverted repeat sequences stimulate slipped misalignment at flanking direct repeats, facilitating deletion of the inverted repeats and one direct repeat. The stimulatory effect is due to formation of a hairpin structure by the inverted repeats, which can both block replication and increase the local proximity of the direct repeats.

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25
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Image of Figure 7
Figure 7

SSA mechanism for deletion formation. Breakage of the chromosome, followed by degradation of one of the two strands at the broken end, will reveal complementary sequences at direct repeats flanking the break. These complementary sequences anneal and are processed to form a deletion between the direct repeats. The initial break may be caused by random breakage due to spontaneous DNA damage (A) or may be induced more efficiently by endonucleolytic cleavage by SbcCD at cruciform structures formed from inverted repeats (B).

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25
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Image of Figure 8
Figure 8

Transposon excision. After transposition, short targetsite duplications flank large inverted repeats at the transposon ends. Formation of a hairpin structure at the inverted repeats can promote deletion at the flanking direct repeats by stimulation of replication slippage. Breakage followed by SSA can also promote excision. For wild-type Tn, mismatches within the inverted ends prompt mismatch repair to destroy the hairpin, thereby reducing the efficiency of transposon excision.

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25
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Image of Figure 9
Figure 9

Quasipalindrome-associated mutation. Strand-switch replication leads to the templating of mutational changes at imperfect or quasipalindrome sequences. Two strand-switch reactions are required to recover products. (A) Simple intramolecular pairing. (B) Intermolecular cross-fork mispairing. Note that this strand switch produces an inversion of the sequence lying between the direct repeats. The product of both intramolecular and intermolecular strand switching is a more perfect (and potentially longer) inverted repeat.

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25
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Image of Figure 10
Figure 10

Inversion by reciprocal cross-fork strand switching. Strand switching of both nascent strands across the fork at inverted repeat sequences causes an inversion of the interval between the inverted repeats (marked with a triangle) and is associated with an inverted duplication of the entire replicon.

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25
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Tables

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Table 1

Genes affecting transposon excision in

Citation: Lovett S. 2005. Misalignment-Mediated Mutations and Genetic Rearrangements at Repetitive DNA Sequences, p 449-464. In Higgins N (ed), The Bacterial Chromosome. ASM Press, Washington, DC. doi: 10.1128/9781555817640.ch25

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