In plants, exposure to solar ultraviolet (UV) light is unavoidable, resulting in 
DNA damage. Damaged DNA causes mutations, replication arrest, and cell death, 
thus efficient repair of the damaged DNA is essential. A light-independent DNA 
repair pathway called nucleotide excision repair (NER) is conserved throughout 
evolution. For example, the damaged DNA-binding protein Radiation sensitive 4 
(Rad4) in Saccharomyces cerevisiae is homologous to the mammalian NER protein 
Xeroderma Pigmentosum complementation group C (XPC). In this study, we examined 
the role of the Arabidopsis thaliana Rad4/XPC homologue (AtRAD4) in plant UV 
tolerance by generating overexpression lines. AtRAD4 overexpression, both with 
and without an N-terminal yellow fluorescent protein (YFP) tag, resulted in 
increased UV tolerance. YFP-RAD4 localized to the nucleus, and UV treatment did 
not alter this localization. We also used yeast two-hybrid analysis to examine 
the interaction of AtRAD4 with Arabidopsis RAD23 and found that RAD4 interacted 
with RAD23B as well as with the structurally similar protein HEMERA (HMR). In 
addition, we found that hmr and rad23 mutants exhibited increased UV 
sensitivity. Thus, our analysis suggests a role for RAD4 and RAD23/HMR in plant 
UV tolerance.