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Chapter 1 : Mutagenesis and DNA Repair: The Consequences of Error and Mechanisms for Remaining the Same

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Mutagenesis and DNA Repair: The Consequences of Error and Mechanisms for Remaining the Same, Page 1 of 2

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Abstract:

The evolution of any species is defined by an accumulation of hereditary changes over time. This chapter talks about a subset of the processes that contribute to change and stability in the prokaryotic genome to consider the necessary balance that exists between the two processes and to discuss circumstances under which a high mutation rate may be necessary for adaptive evolution. Spontaneous mutation rates are remarkably similar among DNA-based microbes. DNA replication is the most significant source of genome stability in an organism. Given the fundamental role of DNA in information storage and hereditary transmission of that information, it seems counterintuitive that this molecule is relatively unstable chemically. Two processes associated with the decay of DNA in vivo are of particular concern when considering spontaneous mutagenesis: depurination and deamination. Numerous mechanisms can contribute to genetic change by altering the DNA molecule. These modifications, if left uncorrected, can direct the replicative polymerase to rewrite the genome, creating a novel draft of the original sequence. Cellular strategies for maintaining genome integrity can be classified as mechanisms that maintain the sequence of the template and mechanisms that improve the fidelity of the replicative polymerase. DNA-repair proteins accurately correct DNA damage by either reversing the chemical modification or excising the altered base. A mismatch correction system functioning after replication improves the accuracy of DNA replication by two orders of magnitude. Finally, the chapter talks about accelerating the pace of evolution as needed.

Citation: Battista J, Earl A. 2004. Mutagenesis and DNA Repair: The Consequences of Error and Mechanisms for Remaining the Same, p 3-20. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch1

Key Concept Ranking

DNA Synthesis
0.740441
DNA Damage and Repair
0.6507377
DNA Polymerase V
0.5161133
DNA Polymerase III
0.5103511
0.740441
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Figures

Image of FIGURE 1
FIGURE 1

Overview of mutagenesis and DNA repair. Native DNA is subjected to endogenous and exogenous sources of DNA damage. The nature of the damage determines the repair pathways activated to counteract these lesions. Failure to accurately restore the wild-type sequence has potentially lethal or mutagenic consequences. MMR, methyl-directed mismatch repair.

Citation: Battista J, Earl A. 2004. Mutagenesis and DNA Repair: The Consequences of Error and Mechanisms for Remaining the Same, p 3-20. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch1
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Image of FIGURE 2
FIGURE 2

Simplified diagrammatic representation of three types of excision repair. (A) Base-excision repair (BER). The modified base is removed by a lesion specific glycosylase and an AP site created by the action of AP endonuclease and DNA deoxyribophosphodiesterase. This 1-bp gap is filled in by DNA polymerase I. (B) Nucleotide-excision repair (NER). A UvrAB complex recognizes distortions in the DNA helix and recruits the UvrC protein to the damaged base. UvrC initiates a bimodal incision. The UvrD helicase releases the damaged fragment leaving a 12- to 13-bp gap. The gap is filled in by DNA polymerase I. (C) Alternative excision repair (AER). A UV DNA damage endonuclease recognizes the lesion and cleaves the phosphate backbone directly 5′ to the lesion. The remaining repair is carried out either by enzymes that unwind the damaged substrate, resulting in a “flap” that is acted on by a flap endonuclease, or by exonucleases that degrade the damaged fragment. DNA synthesis fills the resulting gap.

Citation: Battista J, Earl A. 2004. Mutagenesis and DNA Repair: The Consequences of Error and Mechanisms for Remaining the Same, p 3-20. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch1
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Image of FIGURE 3
FIGURE 3

Daughter-strand gap repair. The lesion, represented here as a thymine dirner, blocks DNA replication in one strand of the duplex. Replication proceeds in the sister strand. DNA replication is reinitiated downstream of the lesion creating a single-strand gap. This gap is filled by a multistep process involving RecA-mediated strand exchange. The intermediates formed are identical with those observed during homologous recombination. The thick black lines represent the parental strands including the damaged strand. The dotted black lines represent daughter-strand DNA synthesized after damage. Branch migration followed by incision at either a or b resolves the structure, yielding two intact DNA molecules. The dimer can now be corrected by excision repair. (Adapted from .)

Citation: Battista J, Earl A. 2004. Mutagenesis and DNA Repair: The Consequences of Error and Mechanisms for Remaining the Same, p 3-20. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch1
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Image of FIGURE 4
FIGURE 4

Diagrammatic representation of methyl-directed mismatch repair in E. coli. Black lines represent newly synthesized DNA duplex. Dotted black lines represent synthesis by DNA polymerase III after mismatch correction. The DNA-damage surveillance protein, MutS, recruits MutL and MutH to the site of the mismatch. In the presence of ATP these proteins catalyze the loop formation, which brings the nearest methylated GATC site in contact with the endonuclease MutH. MutH discriminates between template and newly synthesized daughter strands and nicks the strand opposite the methylated site. The nicked DNA is then acted on by the helicase, UvrD, and directional exonucleases that unwind and degrade the unmethylated daughter strand. Resynthesis is carried out by DNA polymerase III. (Adapted from .)

Citation: Battista J, Earl A. 2004. Mutagenesis and DNA Repair: The Consequences of Error and Mechanisms for Remaining the Same, p 3-20. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch1
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References

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Tables

Generic image for table
TABLE 1

Reported error rates for purified prokaryotic DNA polymerases

Citation: Battista J, Earl A. 2004. Mutagenesis and DNA Repair: The Consequences of Error and Mechanisms for Remaining the Same, p 3-20. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch1
Generic image for table
TABLE 2

Characterized DNA glycosylases and their substrates

Citation: Battista J, Earl A. 2004. Mutagenesis and DNA Repair: The Consequences of Error and Mechanisms for Remaining the Same, p 3-20. In Miller R, Day M (ed), Microbial Evolution. ASM Press, Washington, DC. doi: 10.1128/9781555817749.ch1

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