Postreplication repair

The DNA bases that contain amino groups tend to deaminate spontaneously. In particular, cytosine significantly deaminates to uracil, but adenine and guanine can also deaminate to hypoxanthine and xanthine, respectively. If not corrected, the new bases can cause serious mutations 

Defects have been found in these mechanisms that cause various human diseases. For example, patients with the genetic disease xeroderma pigmentosum are especially sensitive to ultraviolet light and develop skin cancer. Skin fibroblasts cultured from these patients have been shown to be defective in DNA repair. 

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VAN DER Laan, R., et al., Characterization of mRAD18Sc, a mouse homolog of the yeast postreplication repair gene RAD18. Genomics, 2000, 69(1), 86-94. 

More recently, Merz et have studied the circulating lymphocytes of humans experimentally exposed to ozone at 0.5 ppm for 6-10 h. A statistically significant increase in the number of minor chromosomal abnormalities (not breaks) was observed it reached a peak about 2 weeks after exposure and later returned to normal. This delay in the development of chromosomal abnormalities observed after ozone exposure in both hamsters and humans differs from that observed in human radiation studies, in which aberrations tend to remain roughly constant over 3-4 weeks. This raises the possibility that the ozone-induced abnormality is related to a postreplication repair process. 

DNA adducts most likely reflects increased DNA repair such as nucleotide excision repair and postreplication repair including translesion synthesis, gap filling, and template switching during replication (27,28). 

RECOMBINATIONAL REPAIR Repair by recombination between sister DNA molecules that fills the gaps opposite unrepaired lesions left in the daughter ENA strands after replication of damaged DNA. (See also POSTREPLICATION REPAIR)... 

Park, S.D., and J.E. Cleaver. Postreplication repair Questions of its definicition and possible alteration in xeroderma pigmentosum cell strains. 

Despite the complexity of DNA replication in E. coli, as well as its rate (as high as 1000 base pairs per second per replication fork), this process is amazingly accurate (approximately one error per 109 to 1010 base pairs per generation). This low error rate is largely a consequence of the precise nature of the copying process itself (i.e., complementary base pairing). However, both pol III and pol I also proofread newly synthesized DNA. Most mispaired nucleotides are removed (by the 3 — 5 exonuclease activities of pol III and pol I) and then replaced. Several postreplication repair mechanisms also contribute to the low error rate in DNA replication. 

See also Pyrimidine Dimers, Thymine Dimers Photoreactivation, Postreplication Repair, RecA / SOS Response, Antioxidants (from Chapter 15), Oxygen Metabolism and Human Disease... 

See also Postreplication Repair, Recombinational Repair, Prokaryotic Mismatch Repair, Eukaryotic Mismatch Repair, SOS Regulon (from Chapter 26)... 

Postreplication repair refers to processes that attempt to fix mismatches, gaps, or damage to DNA that escape the repair processes that occur during replication (such as proofreading—see here). 

Another postreplication repair system is that of mismatch repair, which can repair replication mistakes that escape proofreading or which arise from chemical alteration of bases, such as deamination of cytosine to form uracil. 

See also Eukaryotic Mismatch Repair, Postreplication Repair... 

Postreplication Repair Recombinational Repair and the SOS Response (Item 1, p. 919) Recombinational Repair (Figure 25.15)... 

Postreplication repair using complementary strand from another DNA molecule... 

McDonald, J. P., Levine, A. S., and Woodgate, R. (1997). The Saccharomyces cerevisiae RAD30 gene, a homologue of Escherichia coli dinB and umuC, is DNA damage inducible and functions in a novel error-free postreplication repair mechanism. Genetics 147, 1557-1568. 

Murakumo, Y, Ogura, Y, Ishii, H., Numata, S.-I., Ichihara, M., Croce, G. M., Fishel, R., and Takahashi, M. (2001). Interactions in the error-prone postreplication repair proteins hREVl, hREV3, and hREV7./. Biol Chem. 276, 35644-35651. 

Fig. 1. Comparison of the DNA postreplication repair response in prokaryotes and eukaryotes. Shaded blocks indicate functionally conserved steps between the Escherichia coli and Saccharomyces cerevisiae pathways.

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