THE SACCHAROMYCES-CEREVISIAE GENE PSO5 RAD16 IS INVOLVED IN THE REGULATION OF DNA-DAMAGE INDUCIBLE GENES RNR2 AND RNR3/

The expression of beta-galactosidase from DNA damage-inducible RNR2-la cZ and RNR3-lacZ fusion constructs was compared in wild-type (WT) and pso5/rad16 mutant strains after treatment with five mutagens/oxidative stressors. While exposure to the mutagens UVC, 4NQO and H2O2 induced expression of the RNR2-lacZ and RNR3-lacZ fusion constructs in two WT strains, treatment with the two oxidative stressors tBOOH and paraquat did not. In the pso5-1 mutant induction of RNR2-lacZ was largely redu ced after UVC and H2O2 while there was no significant induction of bet a-galactosidase expression after 4NQO treatment for this construct. Fo r RNR3-lacZ there was strongly reduced expression of pso5-1 after UVC and 4NQO while H2O2 failed to induce expression of beta-galactosidase. In the WT strains the ranking of the inducing power of the mutagens a t 90% survival las measured in the pso5-1 mutant) was 4NQO > UVC > H2O 2. Though the WT strains were clearly more resistant that the pso5-l m utant to the two oxidative stressors paraquat and tBOOH, these substan ces failed to significantly enhance expression of the RNR2-lacZ and RN R3-lacZ fusion constructs in both the WT and the pso5-l mutant. Our da ta suggest that PsoSp/Rad16p has a function in the signal transducing pathway controlling DNA damage-inducible components of nucleotide exci sion repair.