Prakash L
Mol Gen Genet. 1981;184(3):471-8. doi: 10.1007/BF00352525.
Postreplication repair of nuclear DNA was examined in an excision defective haploid strain of yeast lacking mitochondrial DNA (rad1 rho 0). The size of the DNA synthesized in cells exposed to various fluences of ultraviolet light (UV) corresponds approximately to the average interdimer distance in the parental DNA. Upon further incubation of cells following exposure to 2.5 J/m2, the DNA increases in size; by 4 h, it corresponds to DNA from uniformly labeled cells. The alkaline sucrose sedimentation pattern of DNA pulse labeled at various times after UV irradiation, for up to 4 h, does not change substantially, indicating that dimers continue to block DNA replication. A significant amount of postreplication repair requires de novo protein synthesis, as determined by its inhibition by cycloheximide. The rad6 mutant does not carry out postreplication repair, the rad18 and rad52 mutants show great inhibition while the rev3 mutation does not affect postreplication repair. Both recombinational and nonrecombinational repair mechanisms may function in postreplication repair and most of postreplication repair is error free.
在缺乏线粒体DNA的酵母切除缺陷单倍体菌株(rad1 rho 0)中检测了核DNA的复制后修复。暴露于不同紫外线(UV)剂量的细胞中合成的DNA大小大约对应于亲本DNA中平均二聚体间距。在暴露于2.5 J/m2后对细胞进行进一步孵育,DNA大小增加;到4小时时,它对应于来自均匀标记细胞的DNA。紫外线照射后长达4小时内不同时间脉冲标记的DNA的碱性蔗糖沉降模式基本不变,表明二聚体继续阻碍DNA复制。如通过环己酰亚胺抑制所确定的,大量的复制后修复需要从头合成蛋白质。rad6突变体不进行复制后修复,rad18和rad52突变体表现出很大的抑制作用,而rev3突变不影响复制后修复。重组和非重组修复机制可能在复制后修复中起作用,并且大多数复制后修复是无差错的。