Abstract
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.
Highlights
All living organisms have an inherent ability to protect their genetic integrity against naturally occurring environmental mutagens
We examined the role of the Arabidopsis thaliana Radiation sensitive 4 (Rad4)/Xeroderma Pigmentosum complementation group C (XPC) homologue (AtRAD4) in plant UV tolerance by generating overexpression lines
Since RAD4 interacted with HMR and RAD23b, we examined the role of HMR and the RAD23 family in Arabidopsis UV tolerance
Summary
All living organisms have an inherent ability to protect their genetic integrity against naturally occurring environmental mutagens. Ultraviolet (UV) light is one of the most common and unavoidable environmental sources of DNA damage. UV induces dipyrimidine photolesions in DNA, such as cyclobutane pyrimidine dimers (CPDs) and 6–4 photoproducts (6–4PPs) [1]. Damaged DNA arrests cellular processes such as replication and transcription. A failure to repair DNA damage leads to disturbances of gene expression, mutations, and apotosis. The mechanisms for the protection and repair of DNA are well-conserved [2]. The single-step light-dependent damage repair, called photoreactivation, is carried out by photolyase enzymes in the presence of blue light.
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