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Nucleotide Excision Repair in Caenorhabditis elegans

DOI: 10.4061/2011/542795

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Abstract:

Nucleotide excision repair (NER) plays an essential role in many organisms across life domains to preserve and faithfully transmit DNA to the next generation. In humans, NER is essential to prevent DNA damage-induced mutation accumulation and cell death leading to cancer and aging. NER is a versatile DNA repair pathway that repairs many types of DNA damage which distort the DNA helix, such as those induced by solar UV light. A detailed molecular model of the NER pathway has emerged from in vitro and live cell experiments, particularly using model systems such as bacteria, yeast, and mammalian cell cultures. In recent years, the versatility of the nematode C. elegans to study DNA damage response (DDR) mechanisms including NER has become increasingly clear. In particular, C. elegans seems to be a convenient tool to study NER during the UV response in vivo, to analyze this process in the context of a developing and multicellular organism, and to perform genetic screening. Here, we will discuss current knowledge gained from the use of C. elegans to study NER and the response to UV-induced DNA damage. 1. DNA Damage Response Mechanisms To preserve and faithfully transmit DNA to the next generation, cells are equipped with a variety of DNA repair pathways and associated DNA damage responses, collectively referred to as the DNA damage response (DDR). DNA is continuously damaged by environmental and metabolism-derived genotoxic agents. It is vital for cells and organisms to properly cope with DNA damage, because unrepaired damage can give rise to mutation and cell death. The importance of the DDR is illustrated by several human cancer prone and/or progeroid hereditary diseases, which are based on defects in the DDR. Over the last decades, a wealth of information on the molecular mechanism of different repair pathways has been gathered from detailed in vitro and live cell studies. Currently, this acquired knowledge is being used to develop therapeutic strategies to treat patients suffering from the consequences of unrepaired DNA damage, such as cancer and aging [1]. Damage is repaired by different DNA repair pathways depending on the type of DNA lesion, genomic location, and the cell cycle phase (for reviews see [2–4]). Lesions originating from different genotoxic sources can range from small base modifications to double-strand breaks. Small base modifications, such as oxidative lesions which do not substantially distort the double helix, are repaired by base excision repair (BER). BER removes single or several bases and repairs the gap by DNA synthesis. Bigger

References

[1]  D. S. Boss, J. H. Beijnen, and J. H. Schellens, “Inducing synthetic lethality using PARP inhibitors,” Current Clinical Pharmacology, vol. 5, no. 3, pp. 192–195, 2010.
[2]  J. Essers, W. Vermeulen, and A. B. Houtsmuller, “DNA damage repair: anytime, anywhere?” Current Opinion in Cell Biology, vol. 18, no. 3, pp. 240–246, 2006.
[3]  S. P. Jackson and J. Bartek, “The DNA-damage response in human biology and disease,” Nature, vol. 461, no. 7267, pp. 1071–1078, 2009.
[4]  G. Giglia-Mari, A. Zotter, and W. Vermeulen, “DNA damage response,” Cold Spring Harbor Perspectives in Biology, vol. 3, Article ID a000745, 2011.
[5]  B. B. Lemmens and M. Tijsterman, “DNA double-strand break repair in Caenorhabditis elegans,” Chromosoma, vol. 120, no. 1, pp. 1–21, 2010.
[6]  N. O'Neil and A. Rose, “DNA repair,” WormBook, pp. 1–12, 2006.
[7]  J. L. Youds, L. J. Barber, and S. J. Boulton, “C. elegans: a model of Fanconi anemia and ICL repair,” Mutation Research, vol. 668, no. 1-2, pp. 103–116, 2009.
[8]  Y. Matsumura and H. N. Ananthaswamy, “Toxic effects of ultraviolet radiation on the skin,” Toxicology and Applied Pharmacology, vol. 195, no. 3, pp. 298–308, 2004.
[9]  J. Cadet, E. Sage, and T. Douki, “Ultraviolet radiation-mediated damage to cellular DNA,” Mutation Research, vol. 571, no. 1-2, pp. 3–17, 2005.
[10]  J. R. Mitchell, J. H. Hoeijmakers, and L. J. Niedernhofer, “Divide and conquer: nucleotide excision repair battles cancer and ageing,” Current Opinion in Cell Biology, vol. 15, no. 2, pp. 232–240, 2003.
[11]  S. Prakash and L. Prakash, “Nucleotide excision repair in yeast,” Mutation Research, vol. 451, no. 1-2, pp. 13–24, 2000.
[12]  L. C. Gillet and O. D. Scharer, “Molecular mechanisms of mammalian global genome nucleotide excision repair,” Chemical Reviews, vol. 106, no. 2, pp. 253–276, 2006.
[13]  P. C. Hanawalt and G. Spivak, “Transcription-coupled DNA repair: two decades of progress and surprises,” Nature Reviews Molecular Cell Biology, vol. 9, no. 12, pp. 958–970, 2008.
[14]  J. Q. Svejstrup, “Contending with transcriptional arrest during RNAPII transcript elongation,” Trends in Biochemical Sciences, vol. 32, no. 4, pp. 165–171, 2007.
[15]  M. Fousteri, W. Vermeulen, A. A. van Zeeland, and L. H. Mullenders, “Cockayne syndrome A and B proteins differentially regulate recruitment of chromatin remodeling and repair factors to stalled RNA polymerase II in vivo,” Molecular Cell, vol. 23, no. 4, pp. 471–482, 2006.
[16]  K. A. Henning, L. Li, N. Iyer et al., “The Cockayne syndrome group A gene encodes a WD repeat protein that interacts with CSB protein and a subunit of RNA polymerase II TFIIH,” Cell, vol. 82, no. 4, pp. 555–564, 1995.
[17]  C. Troelstra, A. van Gool, J. de Wit, W. Vermeulen, D. Bootsma, and J. H. Hoeijmakers, “ERCC6, a member of a subfamily of putative helicases, is involved in Cockayne's syndrome and preferential repair of active genes,” Cell, vol. 71, no. 6, pp. 939–953, 1992.
[18]  A. J. van Gool, R. Verhage, S. M. Swagemakers et al., “RAD26, the functional S.cerevisiae homolog of the cockayne syndrome B gene ERCC6,” The EMBO Journal, vol. 13, no. 22, pp. 5361–5369, 1994.
[19]  M. Araki, C. Masutani, M. Takemura et al., “Centrosome protein centrin 2/caltractin 1 is part of the xeroderma pigmentosum group C complex that initiates global genome nucleotide excision repair,” Journal of Biological Chemistry, vol. 276, no. 22, pp. 18665–18672, 2001.
[20]  K. Sugasawa, J. M. Ng, C. Masutani et al., “Xeroderma pigmentosum group C protein complex is the initiator of global genome nucleotide excision repair,” Molecular Cell, vol. 2, no. 2, pp. 223–232, 1998.
[21]  M. Wakasugi, A. Kawashima, H. Morioka et al., “DDB accumulates at DNA damage sites immediately after UV irradiation and directly stimulates nucleotide excision repair,” Journal of Biological Chemistry, vol. 277, no. 3, pp. 1637–1640, 2002.
[22]  R. Groisman, J. Polanowska, I. Kuraoka et al., “The ubiquitin ligase activity in the DDB2 and CSA complexes is differentially regulated by the COP9 signalosome in response to DNA damage,” Cell, vol. 113, no. 3, pp. 357–367, 2003.
[23]  K. Sugasawa, Y. Okuda, M. Saijo et al., “UV-induced ubiquitylation of XPC protein mediated by UV-DDB-ubiquitin ligase complex,” Cell, vol. 121, no. 3, pp. 387–400, 2005.
[24]  H. Wang, L. Zhai, J. Xu et al., “Histone H3 and H4 ubiquitylation by the CUL4-DDB-ROC1 ubiquitin ligase facilitates cellular response to DNA damage,” Molecular Cell, vol. 22, no. 3, pp. 383–394, 2006.
[25]  J. H. Min and N. P. Pavletich, “Recognition of DNA damage by the Rad4 nucleotide excision repair protein,” Nature, vol. 449, no. 7162, pp. 570–575, 2007.
[26]  S. N. Guzder, P. Sung, L. Prakash, and S. Prakash, “Affinity of yeast nucleotide excision repair factor 2, consisting of the Rad4 and Rad23 proteins, for ultraviolet damaged DNA,” Journal of Biological Chemistry, vol. 273, no. 47, pp. 31541–31546, 1998.
[27]  T. G. Gillette, S. Yu, Z. Zhou, R. Waters, S. A. Johnston, and S. H. Reed, “Distinct functions of the ubiquitin-proteasome pathway influence nucleotide excision repair,” The EMBO Journal, vol. 25, no. 11, pp. 2529–2538, 2006.
[28]  M. Volker, M. J. Mone, P. Karmakar et al., “Sequential assembly of the nucleotide excision repair factors in vivo,” Molecular Cell, vol. 8, no. 1, pp. 213–224, 2001.
[29]  M. Yokoi, C. Masutani, T. Maekawa, K. Sugasawa, Y. Ohkuma, and F. Hanaoka, “The xeroderma pigmentosum group C protein complex XPC-HR23B plays an important role in the recruitment of transcription factor IIH to damaged DNA,” Journal of Biological Chemistry, vol. 275, no. 13, pp. 9870–9875, 2000.
[30]  K. Sugasawa, J. Akagi, R. Nishi, S. Iwai, and F. Hanaoka, “Two-step recognition of DNA damage for mammalian nucleotide excision repair: directional binding of the XPC complex and DNA strand scanning,” Molecular Cell, vol. 36, no. 4, pp. 642–653, 2009.
[31]  W. L. de Laat, E. Appeldoorn, K. Sugasawa, E. Weterings, N. G. Jaspers, and J. H. Hoeijmakers, “DNA-binding polarity of human replication protein A positions nucleases in nucleotide excision repair,” Genes and Development, vol. 12, no. 16, pp. 2598–2609, 1998.
[32]  J. C. Huang, D. L. Svoboda, J. T. Reardon, and A. Sancar, “Human nucleotide excision nuclease removes thymine dimers from DNA by incising the 22nd phosphodiester bond 5' and the 6th phosphodiester bond 3' to the photodimer,” Proceedings of the National Academy of Sciences of the United States of America, vol. 89, no. 8, pp. 3664–3668, 1992.
[33]  A. O'Donovan, A. A. Davies, J. G. Moggs, S. C. West, and R. D. Wood, “XPG endonuclease makes the 3' incision in human DNA nucleotide excision repair,” Nature, vol. 371, no. 6496, pp. 432–435, 1994.
[34]  A. M. Sijbers, W. L. de Laat, R. R. Ariza et al., “Xeroderma pigmentosum group F caused by a defect in a structure-specific DNA repair endonuclease,” Cell, vol. 86, no. 5, pp. 811–822, 1996.
[35]  R. M. Overmeer, A. M. Gourdin, A. Giglia-Mari et al., “Replication factor C recruits DNA polymerase delta to sites of nucleotide excision repair but is not required for PCNA recruitment,” Molecular and Cellular Biology, vol. 30, no. 20, pp. 4828–4839, 2010.
[36]  J. Moser, H. Kool, I. Giakzidis, K. Caldecott, L. H. Mullenders, and M. I. Fousteri, “Sealing of chromosomal DNA nicks during nucleotide excision repair requires XRCC1 and DNA ligase IIIα in a cell-cycle-specific manner,” Molecular Cell, vol. 27, no. 2, pp. 311–323, 2007.
[37]  T. Ogi, S. Limsirichaikul, R. M. Overmeer et al., “Three DNA polymerases, recruited by different mechanisms, carry out NER repair synthesis in human cells,” Molecular Cell, vol. 37, no. 5, pp. 714–727, 2010.
[38]  J. H. Hoeijmakers, “DNA damage, aging, and cancer,” The New England Journal of Medicine, vol. 361, no. 15, pp. 1475–1485, 2009.
[39]  L. J. Niedernhofer, “Nucleotide excision repair deficient mouse models and neurological disease,” DNA Repair, vol. 7, no. 7, pp. 1180–1189, 2008.
[40]  N. G. Jaspers, A. Raams, M. C. Silengo et al., “First reported patient with human ERCC1 deficiency has cerebro-oculo-facio- skeletal syndrome with a mild defect in nucleotide excision repair and severe developmental failure,” The American Journal of Human Genetics, vol. 80, no. 3, pp. 457–466, 2007.
[41]  L. J. Niedernhofer, G. A. Garinis, A. Raams et al., “A new progeroid syndrome reveals that genotoxic stress suppresses the somatotroph axis,” Nature, vol. 444, no. 7122, pp. 1038–1043, 2006.
[42]  J. J. Sekelsky, M. H. Brodsky, and K. C. Burtis, “DNA repair in Drosophila: insights from the Drosophila genome sequence,” Journal of Cell Biology, vol. 150, no. 2, pp. F31–F36, 2000.
[43]  J. P. Mueller and M. J. Smerdon, “Rad23 is required for transcription-coupled repair and efficient overall repair in Saccharomyces cerevisiae,” Molecular and Cellular Biology, vol. 16, no. 5, pp. 2361–2368, 1996.
[44]  R. A. Verhage, A. M. Zeeman, M. Lombaerts, P. van de Putte, and J. Brouwer, “Analysis of gene- and strand-specific repair in the moderately UV-sensitive Saccharomyces cerevisiae rad23mutant,” Mutation Research, vol. 362, no. 2, pp. 155–165, 1996.
[45]  H. de Waard, E. Sonneveld, J. de Wit et al., “Cell-type-specific consequences of nucleotide excision repair deficiencies: embryonic stem cells versus fibroblasts,” DNA Repair, vol. 7, no. 10, pp. 1659–1669, 2008.
[46]  T. Nouspikel, “DNA repair in mammalian cells: nucleotide excision repair: variations on versatility,” Cellular and Molecular Life Sciences, vol. 66, no. 6, pp. 994–1009, 2009.
[47]  A. P. Eker, C. Quayle, I. Chaves, and G. T. van der Horst, “DNA repair in mammalian cells: direct DNA damage reversal: elegant solutions for nasty problems,” Cellular and Molecular Life Sciences, vol. 66, no. 6, pp. 968–980, 2009.
[48]  M. Budzowska and R. Kanaar, “Mechanisms of dealing with DNA damage-induced replication problems,” Cell Biochemistry and Biophysics, vol. 53, no. 1, pp. 17–31, 2009.
[49]  S. J. Boulton, A. Gartner, J. Reboul et al., “Combined functional genomic maps of the C. elegans DNA damage response,” Science, vol. 295, no. 5552, pp. 127–131, 2002.
[50]  H. Morinaga, S. I. Yonekura, N. Nakamura, H. Sugiyama, S. Yonei, and Q. M. Zhang-Akiyama, “Purification and characterization of Caenorhabditis elegans NTH, a homolog of human endonuclease III: essential role of N-terminal region,” DNA Repair, vol. 8, no. 7, pp. 844–851, 2009.
[51]  N. Nakamura, H. Morinaga, M. Kikuchi et al., “Cloning and characterization of uracil-DNA glycosylase and the biological consequences of the loss of its function in the nematode Caenorhabditis elegans,” Mutagenesis, vol. 23, no. 5, pp. 407–413, 2008.
[52]  A. Shatilla and D. Ramotar, “Embryonic extracts derived from the nematode Caenorhabditis elegans remove uracil from DNA by the sequential action of uracil-DNA glycosylase and AP (apurinic/apyrimidinic) endonuclease,” Biochemical Journal, vol. 365, no. 2, pp. 547–553, 2002.
[53]  N. P. Degtyareva, P. Greenwell, E. R. Hofmann et al., “Caenorhabditis elegans DNA mismatch repair gene msh-2 is required for microsatellite stability and maintenance of genome integrity,” Proceedings of the National Academy of Sciences of the United States of America, vol. 99, no. 4, pp. 2158–2163, 2002.
[54]  M. Tijsterman, J. Pothof, and R. H. A. Plasterk, “Frequent germline mutations and somatic repeat instability in DNA mismatch-repair-deficient Caenorhabditis elegans,” Genetics, vol. 161, no. 2, pp. 651–660, 2002.
[55]  P. S. Hartman and R. K. Herman, “Radiation-sensitive mutants of Caenorhabditis elegans,” Genetics, vol. 102, no. 2, pp. 159–178, 1982.
[56]  P. S. Hartman, “UV irradiation of wild type and radiation-sensitive mutants of the nematode Caenorhabditis elegans: fertilities, survival, and parental effects,” Photochemistry and Photobiology, vol. 39, no. 2, pp. 169–175, 1984.
[57]  P. S. Hartman, “Epistatic interactions of radiation-sensitive (RAD) mutants of Caenorhabditis elegans,” Genetics, vol. 109, no. 1, pp. 81–93, 1985.
[58]  P. S. Hartman, J. Hevelone, V. Dwarakanath, and D. L. Mitchell, “Excision repair of UV radiation-induced DNA damage in Caenorhabditis elegans,” Genetics, vol. 122, no. 2, pp. 379–385, 1989.
[59]  P. S. Hartman, V. J. Simpson, T. Johnson, and D. Mitchell, “Radiation sensitivity and DNA repair in Caenorhabditis elegans strains with different mean life spans,” Mutation Research, vol. 208, no. 2, pp. 77–82, 1988.
[60]  C. A. Jones and P. S. Hartman, “Replication in UV-irradiated Caenorhabditis elegans embryos,” Photochemistry and Photobiology, vol. 63, no. 2, pp. 187–192, 1996.
[61]  P. S. Hartman, “Effects of age and liquid holding on the UV-radiation sensitivities of wild-type and mutant Caenorhabditis elegans dauer larvae,” Mutation Research, vol. 132, no. 3-4, pp. 95–99, 1984.
[62]  S. Ahmed, A. Alpi, M. O. Hengartner, and A. Gartner, “C. elegans RAD-5/CLK-2 defines a new DNA damage checkpoint protein,” Current Biology, vol. 11, no. 24, pp. 1934–1944, 2001.
[63]  J. W. Astin, N. J. O'Neil, and P. E. Kuwabara, “Nucleotide excision repair and the degradation of RNA pol II by the Caenorhabditis elegans XPA and Rsp5 orthologues, RAD-3 and WWP-1,” DNA Repair, vol. 7, no. 2, pp. 267–280, 2008.
[64]  A. H. Holway, S. H. Kim, A. La Volpe, and W. M. Michael, “Checkpoint silencing during the DNA damage response in Caenorhabditis elegans embryos,” Journal of Cell Biology, vol. 172, no. 7, pp. 999–1008, 2006.
[65]  J. N. Meyer, W. A. Boyd, G. A. Azzam, A. C. Haugen, J. H. Freedman, and B. van Houten, “Decline of nucleotide excision repair capacity in aging Caenorhabditis elegans,” Genome Biology, vol. 8, no. 5, article R70, 2007.
[66]  A. Gartner, S. Milstein, S. Ahmed, J. Hodgkin, and M. O. Hengartner, “A conserved checkpoint pathway mediates DNA damage—induced apoptosis and cell cycle arrest in C. elegans,” Molecular Cell, vol. 5, no. 3, pp. 435–443, 2000.
[67]  N. Ishii, N. Suzuki, P. S. Hartman, and K. Suzuki, “The effects of temperature on the longevity of a radiation-sensitive mutant rad-8 of the nematode Caenorhabditis elegans,” Journals of Gerontology, vol. 49, no. 3, pp. B117–B120, 1994.
[68]  M. H. Lee, B. Ahn, I. S. Choi, and H. S. Koo, “The gene expression and deficiency phenotypes of Cockayne syndrome B protein in Caenorhabditis elegans,” FEBS Letters, vol. 522, no. 1-3, pp. 47–51, 2002.
[69]  H. K. Park, D. Suh, M. Hyun, H. S. Koo, and B. Ahn, “A DNA repair gene of Caenorhabditis elegans: a homolog of human XPF,” DNA Repair, vol. 3, no. 10, pp. 1375–1383, 2004.
[70]  H. K. Park, J. S. Yook, H. S. Koo, I. S. Choi, and B. Ahn, “The Caenorhabditis elegans XPA homolog of human XPA,” Molecules and Cells, vol. 14, no. 1, pp. 50–55, 2002.
[71]  H. Lans, J. A. Marteijn, B. Schumacher, J. H. Hoeijmakers, G. Jansen, and W. Vermeulen, “Involvement of global genome repair, transcription coupled repair, and chromatin remodeling in UV DNA damage response changes during development,” PLoS Genetics, vol. 6, Article ID e1000941, 2010.
[72]  L. Stergiou, K. Doukoumetzidis, A. Sendoel, and M. O. Hengartner, “The nucleotide excision repair pathway is required for UV-C-induced apoptosis in Caenorhabditis elegans,” Cell Death and Differentiation, vol. 14, no. 6, pp. 1129–1138, 2007.
[73]  L. Stergiou, R. Eberhard, K. Doukoumetzidis, and M. O. Hengartner, “NER and HR pathways act sequentially to promote UV-C-induced germ cell apoptosis in Caenorhabditis elegans,” Cell Death and Differentiation, vol. 18, pp. 897–906, 2011.
[74]  C. I. Keller, J. Calkins, P. S. Hartman, and C. S. Rupert, “UV photobiology of the nematode Caenorhabditis elegans: action spectra, absence of photoreactivation and effects of caffeine,” Photochemistry and Photobiology, vol. 46, no. 4, pp. 483–488, 1987.
[75]  Y. Kim and E. T. Kipreos, “The Caenorhabditis elegans replication licensing factor CDT-1 is targeted for degradation by the CUL-4/DDB-1 complex,” Molecular and Cellular Biology, vol. 27, no. 4, pp. 1394–1406, 2007.
[76]  J. Hodgkin, H. R. Horvitz, and S. Brenner, “Nondisjunction mutants of the nematode Caenorhabditis elegans,” Genetics, vol. 91, no. 1, pp. 67–94, 1979.
[77]  D. B. Pontier and M. Tijsterman, “A Robust network of double-strand break repair pathways governs genome integrity during C. elegans development,” Current Biology, vol. 19, no. 16, pp. 1384–1388, 2009.
[78]  T. T. Saito, J. L. Youds, S. J. Boulton, and M. P. Colaiacovo, “Caenorhabditis elegans HIM-18/SLX-4 interacts with SLX-1 and XPF-1 and maintains genomic integrity in the germline by processing recombination intermediates,” PLoS Genetics, vol. 5, no. 11, Article ID e1000735, 2009.
[79]  J. L. Youds, N. J. O'Neil, and A. M. Rose, “Homologous recombination is required for genome stability in the absence of DOG-1 in Caenorhabditis elegans,” Genetics, vol. 173, no. 2, pp. 697–708, 2006.
[80]  R. S. Kamath, A. G. Fraser, Y. Dong et al., “Systematic functional analysis of the Caenorhabditis elegans genome using RNAi,” Nature, vol. 421, no. 6920, pp. 231–237, 2003.
[81]  B. S?nnichsen, L. B. Koski, A. Walsh et al., “Full-genome RNAi profiling of early embryogenesis in Caenorhabditis elegans,” Nature, vol. 434, no. 7032, pp. 462–469, 2005.
[82]  T. Ohkumo, C. Masutani, T. Eki, and F. Hanaoka, “Deficiency of the Caenorhabditis elegans DNA polymerase η homologue increases sensitivity to UV radiation during germ-line development,” Cell Structure and Function, vol. 31, no. 1, pp. 29–37, 2006.
[83]  J. Pothof, G. van Haaften, K. Thijssen et al., “Identification of genes that protect the C. elegans genome against mutations by genome-wide RNAi,” Genes and Development, vol. 17, no. 4, pp. 443–448, 2003.
[84]  M. R. Wallenfang and G. Seydoux, “cdk-7 is required for mRNA transcription and cell cycle progression in Caenorhabditis elegansembryos,” Proceedings of the National Academy of Sciences of the United States of America, vol. 99, no. 8, pp. 5527–5532, 2002.
[85]  T. Eki, T. Ishihara, I. Katsura, and F. Hanaoka, “A genome-wide survey and systematic RNAi-based characterization of helicase-like genes in Caenorhabditis elegans,” DNA Research, vol. 14, no. 4, pp. 183–199, 2007.
[86]  M. Hyun, J. Lee, K. Lee, A. May, V. A. Bohr, and B. Ahn, “Longevity and resistance to stress correlate with DNA repair capacity in Caenorhabditis elegans,” Nucleic Acids Research, vol. 36, no. 4, pp. 1380–1389, 2008.
[87]  O. Fensgard, H. Kassahun, I. Bombik, T. Rognes, J. M. Lindvall, and H. Nilsen, “A two-tiered compensatory response to loss of DNA repair modulates aging and stress response pathways,” Aging, vol. 2, no. 3, pp. 133–159, 2010.
[88]  K. Kiontke and W. Sudhaus, “Ecology of Caenorhabditis species,” WormBook, pp. 1–14, 2006.
[89]  E. C. Friedberg, G. C. Walker, W. Siede, et al., DNA Repair and Mutagenesis, ASM Press, Washington, DC, USA, 2006.
[90]  S. Brenner, “The genetics of Caenorhabditis elegans,” Genetics, vol. 77, no. 1, pp. 71–94, 1974.
[91]  D. L. Mitchell, C. A. Haipek, and J. M. Clarkson, “(6-4)photoproducts are removed from the DNA of UV-irradiated mammalian cells more efficiently than cyclobutane pyrimidine dimers,” Mutation Research, vol. 143, no. 3, pp. 109–112, 1985.
[92]  W. A. Boyd, T. L. Crocker, A. M. Rodriguez et al., “Nucleotide excision repair genes are expressed at low levels and are not detectably inducible in Caenorhabditis elegans somatic tissues, but their function is required for normal adult life after UVC exposure,” Mutation Research, vol. 683, no. 1-2, pp. 57–67, 2010.
[93]  D. Greenstein, “Control of oocyte meiotic maturation and fertilization,” WormBook, pp. 1–12, 2005.
[94]  T. L. Gumienny, E. Lambie, E. Hartwieg, H. R. Horvitz, and M. O. Hengartner, “Genetic control of programmed cell death in the Caenorhabditis elegans hermaphrodite germline,” Development, vol. 126, no. 5, pp. 1011–1022, 1999.
[95]  M. Giannattasio, C. Follonier, H. Tourriere et al., “Exo1 competes with repair synthesis, converts NER intermediates to long ssDNA gaps, and promotes checkpoint activation,” Molecular Cell, vol. 40, no. 1, pp. 50–62, 2010.
[96]  J. A. Marteijn, S. Bekker-Jensen, N. Mailand et al., “Nucleotide excision repair-induced H2A ubiquitination is dependent on MDC1 and RNF8 and reveals a universal DNA damage response,” Journal of Cell Biology, vol. 186, no. 6, pp. 835–847, 2009.
[97]  P. Hartman, J. Reddy, and B. A. Svendsen, “Does trans-lesion synthesis explain the UV-radiation resistance of DNA synthesis in C. elegans embryos?” Mutation Research, vol. 255, no. 2, pp. 163–173, 1991.
[98]  C. Masutani, R. Kusumoto, A. Yamada et al., “The XPV (xeroderma pigmentosum variant) gene encodes human DNA polymerase eta,” Nature, vol. 399, no. 6737, pp. 700–704, 1999.
[99]  S. H. Kim and W. M. Michael, “Regulated proteolysis of DNA polymerase η during the DNA-damage response in C. elegans,” Molecular Cell, vol. 32, no. 6, pp. 757–766, 2008.
[100]  E. Lozano, A. G. Sáez, A. J. Flemming, A. Cunha, and A. M. Leroi, “Regulation of growth by ploidy in Caenorhabditis elegans,” Current Biology, vol. 16, no. 5, pp. 493–498, 2006.
[101]  C. J. Kenyon, “The genetics of ageing,” Nature, vol. 464, no. 7288, pp. 504–512, 2010.
[102]  I. van der Pluijm, G. A. Garinis, R. M. Brandt et al., “Impaired genome maintenance suppresses the growth hormone—insulin-like growth factor 1 axis in mice with Cockayne syndrome,” PLoS Biology, vol. 5, no. 1, p. e2, 2007.
[103]  P. L. Larsen, “Aging and resistance to oxidative damage in Caenorhabditis elegans,” Proceedings of the National Academy of Sciences of the United States of America, vol. 90, no. 19, pp. 8905–8909, 1993.
[104]  J. R. Vanfleteren, “Oxidative stress and ageing in Caenorhabditis elegans,” Biochemical Journal, vol. 292, no. 2, part 2, pp. 605–608, 1993.
[105]  S. Murakami and T. E. Johnson, “A genetic pathway conferring life extension and resistance to UV stress inCaenorhabditis elegans,” Genetics, vol. 143, no. 3, pp. 1207–1218, 1996.
[106]  T. E. Johnson and P. S. Hartman, “Radiation effects on life span in Caenorhabditis elegans,” Journals of Gerontology, vol. 43, no. 5, pp. B137–B141, 1988.
[107]  B. Schumacher, J. H. Hoeijmakers, and G. A. Garinis, “Sealing the gap between nuclear DNA damage and longevity,” Molecular and Cellular Endocrinology, vol. 112, p. 117, 2009.
[108]  G. A. Garinis, L. M. Uittenboogaard, H. Stachelscheid et al., “Persistent transcription-blocking DNA lesions trigger somatic growth attenuation associated with longevity,” Nature Cell Biology, vol. 11, no. 5, pp. 604–615, 2009.
[109]  P. C. Hanawalt, J. M. Ford, and D. R. Lloyd, “Functional characterization of global genomic DNA repair and its implications for cancer,” Mutation Research, vol. 544, no. 2-3, pp. 107–114, 2003.
[110]  C. Janion, “Inducible SOS response system of DNA repair and mutagenesis in Escherichia coli,” International Journal of Biological Sciences, vol. 4, no. 6, pp. 338–344, 2008.
[111]  Y. Fu, L. Pastushok, and W. Xiao, “DNA damage-induced gene expression in Saccharomyces cerevisiae,” FEMS Microbiology Reviews, vol. 32, no. 6, pp. 908–926, 2008.

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