Neither enhanced removal of cyclobutane pyrimidine dimers nor strand-specific repair is found after transcription induction of the beta 3-tubulin gene in a Drosophila embryonic cell line Kc.

Nucleotide excision repair (NER) of ultraviolet (UV) light induced cyclobutane pyrimidine dimers (CPDs) was assayed in a Drosophila melanogaster Kc subline that responds to treatment with the steroid hormone 20-hydroxyecdysone (20-OH-E; beta-ecdysone, ecdysterone). In this cell line the hormone induces transcription of the beta 3-tubulin gene which is not expressed under standard culture conditions. Cells were exposed to either 10 or 15 J/m2 UV (predominantly 254-nm) and removal of CPDs from several genes, including beta 3-tubulin, and total cellular DNA was assayed. We show that upon induction of transcription of the beta 3-tubulin gene, its repair is not enhanced. In non-treated as well as 20-OH-E treated cells, repair kinetics in beta 3-tubulin resemble those in the active genes Gart and Notch, the inactive locus white and total cellular DNA. Moreover, in the presence as well as in the absence of transcription, the separate strands of the beta 3-tubulin gene are repaired with the same rate and to the same extent: about 90% after 24 h. It can be concluded from these observations that transcription is not a prerequisite for the efficient repair of CPDs in the Drosophila embryonic Kc cell line.