A large UVA dose by itself induces lethal damage revealed in some repair-deficient strains of Saccharomyces cerevisiae. Following photoaddition of a monofunctional psoralen derivative, 3-carbethoxypsoralen, an extra killing effect is observed by applying a second high UVA dose, in conditions where a fraction of 8-methoxypsoralen (8-MOP) plus UVA-induced monoadducts are transformed into DNA cross-links. In an excision-repair-deficient context, the bypass of 8-MOP plus UVA-induced monoadducts is under the control of the RAD6+ gene product. However, when other steps of the mutagenic pathway are blocked by the rad18-2 or the pso1-1 mutations, bypass occurs. This is also true when in excision-deficient strains the recombinogenic pathway is blocked by the rad52-1 mutation. The recombinogenic pathway may be an alternative to the mutagenic pathway for bypass of monoadducts. The repair of the lesions induced by a second UVA dose applied after a first treatment by 8-MOP plus UVA [i.e. cross-links and other putative lesion(s)] is controlled by at least the RAD2+, RAD6+, RAD52+, PSO2+ and PSO1+ gene products. The role of the pathways involved is discussed according to the nature of the secondarily induced lesions.
|Evidence ID||Analyze ID||Interactor||Interactor Systematic Name||Interactor||Interactor Systematic Name||Type||Assay||Annotation||Action||Modification||Phenotype||Source||Reference||Note|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Gene Ontology Term||Gene Ontology Term ID||Qualifier||Aspect||Method||Evidence||Source||Assigned On||Reference||Annotation Extension|
|Evidence ID||Analyze ID||Gene||Gene Systematic Name||Phenotype||Experiment Type||Experiment Type Category||Mutant Information||Strain Background||Chemical||Details||Reference|
|Evidence ID||Analyze ID||Regulator||Regulator Systematic Name||Target||Target Systematic Name||Experiment||Conditions||Strain||Source||Reference|