Slt2 (Mpk1) MAP kinase is involved in the response of Saccharomyces cerevisiae to 8-methoxypsoralen plus UVA.

摘要: Abstract The bifunctional furocoumarin 8-methoxypsoralen (8-MOP) is a well established drug in the photochemotherapy of psoriasis and other skin diseases. In eukaryotic cells, this compound intercalates into DNA undergoes photocycloaddition with pyrimidines to form monoadducts interstrand crosslinks initiating cascade events leading cytotoxic, mutagenic carcinogenic responses. yeast exposure 8-MOP plus UVA induces transcription large set genes, cellular reaction different from an overall damage response specific 8-MOP/UVA [M. Dardalhon, W. Lin, A. Nicolas, D. Averbeck, Specific transcriptional responses induced by yeast, FEMS Yeast Res. 7 (2007) 866–878]. To further define relationship between genes genotoxic consequences after treatment, survival mutants deleted for that are specifically were analysed terms survival. Six RAD51, RAD54, DUN1, DIN7, already known be implicated responses, SLT2/MPK1 PDE2 involved cell wall stress found sensitive treatment. Further characterization slt2 mutant provides evidence existence which Slt2 MAPK pathway implicated. Activation MAP kinase previously observed at level now confirmed protein level. addition sensitivity 8-MOP/UVA, cells lacking SLT2 show reduced 3-carbethoxypsoralen 1,6-dioxapyrene UVA. Osmotic support could suppress sensitivities these agents, suggesting related integrity defects and/or defects.