Table3B.SomeMutagenicandNon-mutagenicRepairProcesses

Table 3B. Some mutagenic and non-mutagenic repair processes

DNA Damage Type or Agent

Error-Free Repair

Error-Prone/

Mutagenic Repair

References

Ionizing radiation, double-strand (DS) breakage, replication fork collapse

Homologous recombination (Rec)

Non-homologous end-joining (NHEJ)

(Cox 2001; Lusetti and Cox 2002; Pastwa and Blasiak 2003; Frankenberg-Schwager, Becker et al. 2008; Fattah, Lee et al. 2010; Grabarz, Barascu et al. 2012)

UV radiation (thymine dimers)

Nucleotide Excision Repair (NER)

Lesion bypass repair

(Petit and Sancar 1999; Tang, Shen et al. 1999; Goodman 2002; Rechkunova and Lavrik 2010)

Alkylation damage

Base excision repair (BER), NER, dealkylation

Lesion bypass repair

(Fromme and Verdine 2004; Robertson, Klungland et al. 2009; Kondo, Takahashi et al. 2010; Jacobs and Schar 2012)

Large chemical adducts

Lesion bypass repair (DNA PolIV & V in E. coli)

(Wagner, Gruz et al. 1999; Napolitano, Janel-Bintz et al. 2000; Goodman 2002)

Oxidative damage

BER

Lesion bypass repair

(Lu, Li et al. 2001; Fromme and Verdine 2004; Yamada, Nunoshiba et al. 2006; Wirtz, Nagel et al. 2010; Jacobs and Schar 2012)

Cytosine deamination to uracil[1]

BER (uracil-N-glycosylase)

BER (uracil-N-glycosylase)

(Jacobs and Schar 2012; Perez-Duran, Belver et al. 2012; Li, Zhao et al. 2013)

REFERENCES

Cox, M. M. (2001). "Recombinational DNA repair of damaged replication forks in Escherichia coli: questions." Annu Rev Genet 35: 53-82. http://www.ncbi.nlm.nih.gov/pubmed/11700277.

Fattah, F., E. H. Lee, et al. (2010). "Ku regulates the non-homologous end joining pathway choice of DNA double-strand break repair in human somatic cells." PLoS Genet 6(2): e1000855. http://www.ncbi.nlm.nih.gov/pubmed/20195511.

Frankenberg-Schwager, M., M. Becker, et al. (2008). "The role of nonhomologous DNA end joining, conservative homologous recombination, and single-strand annealing in the cell cycle-dependent repair of DNA double-strand breaks induced by H(2)O(2) in mammalian cells." Radiat Res 170(6): 784-793. http://www.ncbi.nlm.nih.gov/pubmed/19138034.

Fromme, J. C. and G. L. Verdine (2004). "Base excision repair." Adv Protein Chem 69: 1-41. http://www.ncbi.nlm.nih.gov/pubmed/15588838.

Goodman, M. (2002). "Error-prone repair DNA polymerases in prokaryotes and eukaryotes." Ann Rev Biochem 71: 17-50. http://www.ncbi.nlm.nih.gov/pubmed/12045089.

Grabarz, A., A. Barascu, et al. (2012). "Initiation of DNA double strand break repair: signaling and single-stranded resection dictate the choice between homologous recombination, non-homologous end-joining and alternative end-joining." Am J Cancer Res 2(3): 249-268. http://www.ncbi.nlm.nih.gov/pubmed/22679557.

Jacobs, A. L. and P. Schar (2012). "DNA glycosylases: in DNA repair and beyond." Chromosoma 121(1): 1-20. http://www.ncbi.nlm.nih.gov/pubmed/22048164.

Kondo, N., A. Takahashi, et al. (2010). "DNA damage induced by alkylating agents and repair pathways." J Nucleic Acids 2010: 543531. http://www.ncbi.nlm.nih.gov/pubmed/21113301.

Li, S., Y. Zhao, et al. (2013). "Analysis of Ig gene hypermutation in Ung(-/-)Polh(-/-) mice suggests that UNG and A:T mutagenesis pathway target different U:G lesions." Mol Immunol 53(3): 214-217. http://www.ncbi.nlm.nih.gov/pubmed/22960197.

Lu, A. L., X. Li, et al. (2001). "Repair of oxidative DNA damage: mechanisms and functions." Cell Biochem Biophys 35(2): 141-170. http://www.ncbi.nlm.nih.gov/pubmed/11892789%22.

Lusetti, S. L. and M. M. Cox (2002). "The bacterial RecA protein and the recombinational DNA repair of stalled replication forks." Annu Rev Biochem 71: 71-100. http://www.ncbi.nlm.nih.gov/pubmed/12045091.

Napolitano, R., R. Janel-Bintz, et al. (2000). "All three SOS-inducible DNA polymerases (Pol II, Pol IV and Pol V) are involved in induced mutagenesis." Embo J 19(22): 6259-6265. http://www.ncbi.nlm.nih.gov/pubmed/11080171.

Pastwa, E. and J. Blasiak (2003). "Non-homologous DNA end joining." Acta Biochim Pol 50(4): 891-908. http://www.ncbi.nlm.nih.gov/pubmed/14739985.

Perez-Duran, P., L. Belver, et al. (2012). "UNG shapes the specificity of AID-induced somatic hypermutation." J Exp Med 209(7): 1379-1389. http://www.ncbi.nlm.nih.gov/pubmed/22665573.

Petit, C. and A. Sancar (1999). "Nucleotide excision repair: from E. coli to man." Biochimie 81(1-2): 15-25. http://www.ncbi.nlm.nih.gov/pubmed/10214906.

Rechkunova, N. I. and O. I. Lavrik (2010). "Nucleotide excision repair in higher eukaryotes: mechanism of primary damage recognition in global genome repair." Subcell Biochem 50: 251-277. http://www.ncbi.nlm.nih.gov/pubmed/20012586.

Robertson, A. B., A. Klungland, et al. (2009). "DNA repair in mammalian cells: Base excision repair: the long and short of it." Cell Mol Life Sci\ 66\(6\): 981-993\. http://www.ncbi.nlm.nih.gov/pubmed/19153658%22.

Tang, M., X. Shen, et al. (1999). "UmuD'(2)C is an error-prone DNA polymerase, Escherichia coli pol V." Proc Natl Acad Sci U S A 96(16): 8919-8924. http://www.ncbi.nlm.nih.gov/pubmed/10430871.

Wagner, J., P. Gruz, et al. (1999). "The dinB gene encodes a novel E. coli DNA polymerase, DNA pol IV, involved in mutagenesis." Mol Cell 4(2): 281-286. http://www.ncbi.nlm.nih.gov/pubmed/10488344.

Wirtz, S., G. Nagel, et al. (2010). "Both base excision repair and O6-methylguanine-DNA methyltransferase protect against methylation-induced colon carcinogenesis." Carcinogenesis 31(12): 2111-2117. http://www.ncbi.nlm.nih.gov/pubmed/20732909.

Yamada, M., T. Nunoshiba, et al. (2006). "Involvement of Y-family DNA polymerases in mutagenesis caused by oxidized nucleotides in Escherichia coli." J Bacteriol 188(13): 4992-4995. http://www.ncbi.nlm.nih.gov/pubmed/16788208.

[1] Note that BER removal of uracil from DNA can have both mutation-prevention and mutation–promotion consequences (Perez-Duran, P., L. Belver, et al. (2012). "UNG shapes the specificity of AID-induced somatic hypermutation." J Exp Med 209(7): 1379-1389. http://www.ncbi.nlm.nih.gov/pubmed/22665573, Li, S., Y. Zhao, et al. (2013). "Analysis of Ig gene hypermutation in Ung(-/-)Polh(-/-) mice suggests that UNG and A:T mutagenesis pathway target different U:G lesions." Mol Immunol 53(3): 214-217. http://www.ncbi.nlm.nih.gov/pubmed/22960197.). Resolving what conditions distinguish these two situations is an active topic of investigation.

Table 3B. Some mutagenic and non-mutagenic repair processes
DNA Damage Type or Agent	Error-Free Repair	Error-Prone/ Mutagenic Repair	References
Ionizing radiation, double-strand (DS) breakage, replication fork collapse	Homologous recombination (Rec)	Non-homologous end-joining (NHEJ)	(Cox 2001; Lusetti and Cox 2002; Pastwa and Blasiak 2003; Frankenberg-Schwager, Becker et al. 2008; Fattah, Lee et al. 2010; Grabarz, Barascu et al. 2012)
UV radiation (thymine dimers)	Nucleotide Excision Repair (NER)	Lesion bypass repair	(Petit and Sancar 1999; Tang, Shen et al. 1999; Goodman 2002; Rechkunova and Lavrik 2010)
Alkylation damage	Base excision repair (BER), NER, dealkylation	Lesion bypass repair	(Fromme and Verdine 2004; Robertson, Klungland et al. 2009; Kondo, Takahashi et al. 2010; Jacobs and Schar 2012)
Large chemical adducts		Lesion bypass repair (DNA PolIV & V in E. coli)	(Wagner, Gruz et al. 1999; Napolitano, Janel-Bintz et al. 2000; Goodman 2002)
Oxidative damage	BER	Lesion bypass repair	(Lu, Li et al. 2001; Fromme and Verdine 2004; Yamada, Nunoshiba et al. 2006; Wirtz, Nagel et al. 2010; Jacobs and Schar 2012)
Cytosine deamination to uracil[1]	BER (uracil-N-glycosylase)	BER (uracil-N-glycosylase)	(Jacobs and Schar 2012; Perez-Duran, Belver et al. 2012; Li, Zhao et al. 2013)