Boulton S J, Jackson S P
Wellcome/CRC Institute and Department of Zoology, Cambridge University, UK.
Nucleic Acids Res. 1996 Dec 1;24(23):4639-48. doi: 10.1093/nar/24.23.4639.
Ku is a heterodimer of polypeptides of approximately 70 and 80 kDa (Ku70 and Ku80, respectively) that binds to DNA ends. Mammalian cells lacking Ku are defective in DNA double-strand break (DSB) repair and in site-specific V(D)J recombination. Here, we describe the identification and characterisation of YKU80, the gene for the Saccharomyces cerevisiae Ku80 homologue. Significantly, we find that YKU80 disruption enhances the radiosensitivity of rad52 mutant strains, suggesting that YKU80 functions in a DNA DSB repair pathway that does not rely on homologous recombination. Indeed, through using an in vivo plasmid rejoining assay, we find that YKU80 plays an essential role in illegitimate recombination events that result in the accurate repair of restriction enzyme generated DSBs. Interestingly, in the absence of YKU80function, residual repair operates through an error-prone pathway that results in recombination between short direct repeat elements. This resembles closely a predominant DSB repair pathway in vertebrates. Together, our data suggest that multiple, evolutionarily conserved mechanisms for DSB repair exist in eukaryotes. Furthermore, they imply that Ku binds to DSBs in vivo and promotes repair both by enhancing accurate DNA end joining and by suppressing alternative error-prone repair pathways. Finally, we report that yku80 mutant yeasts display dramatic telomeric shortening, suggesting that, in addition to recognising DNA damage, Ku also binds to naturally occurring chromosomal ends. These findings raise the possibility that Ku protects chromosomal termini from nucleolytic attack and functions as part of a telomeric length sensing system.
Ku是一种由大约70 kDa和80 kDa的多肽组成的异源二聚体(分别为Ku70和Ku80),它能与DNA末端结合。缺乏Ku的哺乳动物细胞在DNA双链断裂(DSB)修复和位点特异性V(D)J重组方面存在缺陷。在此,我们描述了酿酒酵母Ku80同源物基因YKU80的鉴定和特征。重要的是,我们发现破坏YKU80会增强rad52突变菌株的辐射敏感性,这表明YKU80在不依赖同源重组的DNA DSB修复途径中发挥作用。实际上,通过体内质粒重新连接试验,我们发现YKU80在导致限制性酶产生的DSB精确修复的非同源重组事件中起关键作用。有趣的是,在缺乏YKU80功能的情况下,残余修复通过易错途径进行,导致短的直接重复元件之间发生重组。这与脊椎动物中一种主要的DSB修复途径非常相似。总之,我们的数据表明真核生物中存在多种进化上保守的DSB修复机制。此外,这意味着Ku在体内与DSB结合,并通过增强精确的DNA末端连接和抑制替代的易错修复途径来促进修复。最后,我们报告yku80突变酵母表现出明显的端粒缩短,这表明,除了识别DNA损伤外,Ku还与天然存在的染色体末端结合。这些发现增加了Ku保护染色体末端免受核酸酶攻击并作为端粒长度传感系统一部分发挥作用的可能性。