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Nucleotide Excision Repair in Caenorhabditis elegans

DOI: 10.4061/2011/542795

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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


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