Abstract: Progress in understanding of DNA repair starts with the isolation of repair-deficient mutants following by the genetic and molecular analysis and the study of mutant phenotypes. Three new repair-deficient mutants of Chlamydomonas reinhardtii were exposed to complex analysis. They were characterized on the basis of UV- , MNNG- and X-ray- survival and mutagenesis and pyrimidine dimer excision on purpose to include them into repair pathways. The most sensitive strain after mutagens used was uvsN350 in which deficiency in pyrimidine dimer excision was proved. It was established that the strain uvs14 exhibited a very high spontaneous and induced mutability after UV and MNNG while the strain uvsN350 did not mutate. Molecular analysis of pyrimidine dimer excision from DNA of repair deficient strains proved their repair genes involvement in different repair pathways. Genetic analysis revealed that repair-deficiency in mutant strains is determined by various genes, two of which (uvs13, uvs14) were located into the first linkage group.