AtPolλ, A Homolog of Mammalian DNA Polymerase λ in Arabidopsis thaliana, is Involved in the Repair of UV-B Induced DNA Damage Through the Dark Repair Pathway

Plants are constantly exposed to a wide range of environmental genotoxic stress factors including obligatory exposure to UV radiation in sunlight. Here, we report the functional characterization of a DNA repair protein, AtPol lambda, a homolog of mammalian DNA polymerase lambda in Arabidopsis, in relation to its role in repair of UV-B-induced DNA damage during early stages of seedling development. The abundance of the AtPol lambda transcript and the protein levels were distinctly increased in response to UV-B irradiation in 6-day-old wild-type seedlings. Growth of atpol lambda mutant seedlings, deficient in AtPol lambda expression, was more sensitive to UV-B radiation compared with wild-type plants when seeds were exposed to UV-B radiation before germination. The atpol lambda mutants showed accumulation of relatively higher amounts of DNA lesions than wild-type plants following UV-B exposure and were less proficient in repair of UV-induced DNA damage. Increased accumulation of AtPol lambda protein in UV-B-irradiated 6-day-old wild-type seedlings during the dark recovery period has indicated a possible role for the protein in repair of UV-B-induced lesions in the dark. Overexpression of AtPol lambda in the atpol lambda mutant line partially complemented the repair proficiency of UV-B-induced DNA damage. In vitro repair synthesis assays using whole-cell extracts from the wild-type and atpol lambda mutant line have further demonstrated the role of AtPol lambda in repair synthesis of UV-B-damaged DNA in the dark through an excision repair mechanism. Overall, our results have indicated the possible involvement of AtPol lambda in a plant's response for repair of UV-B-mediated DNA damage during seedling development.