DNA damage represents a threat to the livelihood of a cell or organism. This damage must be dealt with in an efficient manner to prevent cell death, or in higher organisms, neoplasia. The study of DNA repair in yeast has been greatly aided by the discovery of radiation-sensitive mutants and their corresponding ' RAD' genes. A loss of function of these 'RAD' or related genes compromises the cell's ability to repair DNA damage. One of the most effective pathways for repairing DNA damage is nucleotide excision repair. Within this pathway, the 'RAD23' gene product plays a crucial, albeit poorly understood role. In this study, three Rad23p-interacting proteins were investigated in order to better understand the role of Rad23p itself. Two of the three proteins investigated were found to be important to cell viability while the remaining protein appeared to be functionally disposable. None of the proteins were found to play a role in DNA repair using the methods in this thesis, suggesting that their interaction with Rad23p is not biologically significant. Alternatively, these genes may be involved with 'RAD23 ' in cellular processes unrelated to DNA repair.