Differential participation of homologous recombination and nucleotide excision repair in yeast survival to ultraviolet light radiation

AimsThe purpose of this research was to assess the ultraviolet light (UV) phenotype of yeast sirΔ cells vs. WT cells, and to determine whether de-silenced chromatin or the intrinsic pseudoploidy of sirΔ mutants contributes to their response to UV. Additional aims were to study the participation of HR and NER in promoting UV survival during the cell cycle, and to define the extent of the co-participation for both repair pathways.Main methodsThe sensitivity of yeast Saccharomyces cerevisiae to UV light was determined using a method based on automatic measurements of optical densities of very small (100 μl) liquid cell cultures.Key findingsWe show that pseudo-diploidy of sirΔ strains promotes resistance to UV irradiation and that HR is the main mechanism that is responsible for this phenotype. In addition, HR together with GG-NER renders cells in the G2-phase of the cell cycle more resistant to UV irradiation than cells in the G1-phase, which underscore the importance of HR when two copies of the chromosomes are present. Nevertheless, in asynchronously growing cells NER is the main repair pathway that responds to UV induced DNA damage.SignificanceThis study provides detailed and quantitative information on the co-participation of HR and NER in UV survival of yeast cells.