Abstract: Chlamydomonas reinhardtii is a convenient model organism for the DNA-repair systems studies in eukaryotic cells. It enables to study repair of both nuclear and extranuclear DNA. The number of DNA-repair studies in Chlamydomonas is small compared to some other eukaryotic microorganisms, e. g. yeast. One of the possible reasons for being behind in the study of DNA-repair in algae was the relatively unsufficient collection of available UV-sensitive (repair-deficient) mutants.

We supplemented the existing collection of UV-sensitive mutants with 11 repair deficient strains as a basic prerequisite for speeding up the study of repair mechanisms in algae. Phenotypic characterization, genetic and molecular analysis of mutants were carried out. Complementation analysis proved that repair-deficient strains being studied were not allelic. The different responses of single and double mutants to UV-light indicated their repair genes involvement in various repair pathways. On the basis of pyrimidine dimer excision from DNA assessment, survival and mutagenesis after UV-light, X-ray, alkylating agents, and recombination activity, the repair-deficient mutants were classified into three separate pathways. Genetic analysis revealed that these repair pathways are determinated by several genes, three of which were located into the first linkage group forming a cluster of repair genes for non-excision DNA repair.

The pleiotropic effect of repair genes including PHR gene has been established. Both in bacteria and in yeast it was proved that photolyase enhanced dark survival of excision proficient strains via specific stimulation of excision repair. To assess the role of photolyase in dark repair in photoautotrophs, double mutants of C. reinhardtii deficient in dark repair and photoreactivation were constructed and assayed for UV sensitivity in different posttreatment light condition. It was found that photolyase may stimulate dark repair processes in C. reinhardtii also via pathway(s) other than nucleotide excision repair.