Plants need sunlight for photosynthesis and survival. However, frequent exposure to solar ultraviolet (UV) rays can damage DNA by inducing dipyrimidine photolesions such as cyclobutane pyrimidine dimers (CPDs) and 6,4 pyrimidine-pyrimidone photoproducts (6-4PPs). These lesions interrupt DNA replication and transcription, leading to mutation and cell death; thus DNA repair is essential. Plants have two mechanisms to repair UV-damaged DNA, one utilizes light (Photoreactivation) and the other does not (Nucleotide Excision Repair (NER)). The plant NER pathway is similar to those in mammals and yeast. In humans, defective or deficient NER causes serious consequences such as xeroderma pigmentosum, where UV-sensitive skin is prone to skin cancer. In mammals, the xeroderma pigmentosum complementation group C (XPC) protein recognizes DNA damage during whole genome NER (global genomic NER (GG-NER)). In this thesis I examine the role of RAD4, the plant homologue of mammalian XPC. RAD4 overexpression lines exhibited increased UV tolerance and YFP-tagged RAD4 localized to the nucleus. RAD4 interacted with RAD23B and the RAD23-like protein HEMERA (HMR) in yeast two hybrid assays and hmr mutants were found to exhibit increased UV sensitivity. In the yeast S. cerevisiae, GG-NER damage recognition is performed by the Rad7p/16p complex. In this study I identified three Arabidopsis RAD7 homologues, RAD7a, RAD7b, and RAD7c. Loss of function alleles in each of the three RAD7 genes led to plants that exhibited increased UV sensitivity, while gain of function lines of RAD7b and RAD7c exhibited increased UV tolerance. YFP-tagged RAD7b and RAD7c localized to the nucleus, and this localization was not affected by UV treatment. Therefore, RAD4 and the three RAD7 homologues contribute to Arabidopsis UV tolerance.