Dark-repair of ultraviolet-induced pyrimidine dimers in the DNA of wild carrot protoplasts

Abstract

GREEN plants receive greater exposure to solar ultraviolet radiation and their germ cells (pollen) have a significantly greater potential for acquiring ultraviolet-induced genetic damage than do those of most animals¹. Even though cells of the higher plants can photoreactivate ultraviolet damage (refs 2–5, and my unpublished data), the absence of dark-repair capability could be a significant disadvantage since some types of excisable ultraviolet-induced DNA damage are not photo-reactivable⁶. The capability for dark repair would become even more important if there were an increase in the fluence of solar ultraviolet reaching the Earth's surface⁷. Attempts to demonstrate excision of pyrimidine dimers in cells of Nicotiana, Haplopappus⁴, Ginkgo⁵ and Chlamydomonas⁸ have all given negative results. These data, taken with other assays for excision repair activity (unscheduled DNA synthesis⁹; repair replication^10–12) have been interpreted as indicating a general absence of such capability in plants¹². I have now found, however, that in cultured wild carrot cells, pyrimidine dimers can be excised in the dark and that the extent of dimer excision depends on the initial number of dimers induced by the ultraviolet dose. After ultraviolet fluences of about 10 J m⁻², most of the dimers are excised within 24 h; but at fluences up to 30 J m⁻², about 25 % remain unexcised in DNA. At fluences above 100 J m⁻², dimer excision is almost completely eliminated, perhaps due to secondary effects of these very high ultraviolet doses.