Drake J W
J Bacteriol. 1985 Jun;162(3):1311-3. doi: 10.1128/jb.162.3.1311-1313.1985.
Photodynamic inactivation of bacteriophage T4 particles, mediated by either angelicin or thiopyronin, is enhanced by defects in the T4 uvsW-uvsX-uvsY postreplication repair system but not by a defect in the denV pyrimidine-dimer-excision system. There was no evidence for functional interactions between the two repair systems. As observed previously with 8-methoxypsoralen, photodynamic mutagenesis with angelicin is abolished by defects in the uvsW-uvsX-uvsY system.
由白芷香豆素或硫代吡喃酮介导的噬菌体T4颗粒的光动力失活,会因T4 uvsW-uvsX-uvsY复制后修复系统的缺陷而增强,但不会因denV嘧啶二聚体切除系统的缺陷而增强。没有证据表明这两种修复系统之间存在功能相互作用。如之前用8-甲氧基补骨脂素所观察到的那样,uvsW-uvsX-uvsY系统的缺陷会消除白芷香豆素的光动力诱变作用。