REMOVAL OF NONHOMOLOGOUS DNA ENDS IN DOUBLE-STRAND BREAK RECOMBINATION - THE ROLE OF THE YEAST ULTRAVIOLET REPAIR GENE RAD1
REMOVAL OF NONHOMOLOGOUS DNA ENDS IN DOUBLE-STRAND BREAK RECOMBINATION - THE ROLE OF THE YEAST ULTRAVIOLET REPAIR GENE RAD1
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DOI：
10.1126/science.1411547
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发表时间：
1992-10-16
期刊：
影响因子：
56.9
通讯作者：
HABER, JE
中科院分区：
文献类型：
--
作者：
FISHMANLOBELL, J;HABER, JE
酿酒酵母中的双链断裂（DSB）可以通过基因转换或通过同源序列的直接重复之间的单链退火导致的缺失来修复。尽管rad 1突变体对X射线具有抵抗力并且可以完成DSB介导的交配型转换，但当断裂末端包含大约60个非同源碱基对时，它们无法完成重组。当断裂的末端与供体序列同源时，突变恢复。此外，RAD1的缺失导致了以前未观察到的重组产物类型的频繁出现。这些数据表明，RAD1需要从重组DNA的3 '端去除非同源DNA，这一过程类似于在修复紫外线损伤的DNA期间切除光二聚体。
Double-strand breaks (DSBs) in Saccharomyces cerevisiae can be repaired by gene conversions or by deletions resulting from single-strand annealing between direct repeats of homologous sequences. Although rad1 mutants are resistant to x-rays and can complete DSB-mediated mating-type switching, they could not complete recombination when the ends of the break contained approximately 60 base pairs of nonhomology. Recombination was restored when the ends of the break were made homologous to donor sequences. Additionally, the absence of RAD1 led to the frequent appearance of a previously unobserved type of recombination product. These data suggest RAD1 is required to remove nonhomologous DNA from the 3' ends of recombining DNA, a process analogous to the excision of photodimers during repair of ultraviolet-damaged DNA.