The pre-UV nutritional stresses increase UV resistance, decrease UV mutagenesis and inhibit excision repair.

Nutritional stresses applied to E. coli prior to UV irradiation increase UV resistance and decrease UV mutagenesis. This effect is uvrA-dependent and might reflect a more efficient excision of pyrimidine dimers [1]. The data presented here, however, indicate that after prestarvation for glucose or amino acids pyrimidine dimer excision (PDE) was partly inhibited. It appears that the stress conditions stimulate a mode of uvr-dependent tolerance of lesions, efficient and precise. Possible modes of PDE inhibition and lesion tolerance are discussed.