Abstract
The most major prevalent lesions produced by ultraviolet (UV) are cyclobutane pyrimidine dimmer and (6-4) photoproducts. These photoproducts impair DNA replication and transcription processes and induce mutation. In higher plants, these photoproducts are thought to be restored with photolyase and nucleotide excision repair (NER). Moreover, it has been thought that these lesions which are not restored by photolyase and NER could be restored by homologous recombination (HR).
In the present study, we have analyzed intra-chromosomal homologous recombination frequency in AtRad1 or AtRad2 knock-out mutant of Arabidopsis. With the result, AtRad1 KO (uvh1) suppress intra-chromosomal homologous recombination, on the other hand AtRad2 KO (uvh3) enhance intra-chromosomal homologous recombination. We have crossed photolyase deficient mutant of Arabidopsis (uvr2-1) with uvh1 or uvh3 to produce double KO mutants, uvr2-1/ uvh1 or uvr2-1/ uvh3, respectively. We are currently analyzing ICHR frequency, UV-sensitivity and accumulation of UV-photoproducts in these double KO mutants.
