Jeggo P A, Taccioli G E, Jackson S P
MRC Cell Mutation Unit, University of Sussex, Brighton, UK.
Bioessays. 1995 Nov;17(11):949-57. doi: 10.1002/bies.950171108.
All organisms possess mechanisms to repair double strand breaks (dsbs) generated in their DNA by damaging agents. Site-specific dsbs are also introduced during V(D)J recombination. Four complementation groups of radiosensitive rodent mutants are defective in the repair of dsbs, and are unable to carry out V(D)J recombination effectively. The immune defect in Severe Combined Immunodeficient (scid) mice also results from an inability to undergo effective V(D)J recombination, and scid cell lines display a repair defect and belong to one of these complementation groups. These findings indicate a mechanistic overlap between the processes of DNA repair and V(D)J recombination. Recently, two of the genes defined by these complementation groups have been identified and shown to encode components of DNA-dependent protein kinase (DNA-PK). We review here the three fields which have become linked by these findings, and discuss the involvement of DNA-PK in dsb rejoining and in V(D)J recombination.
所有生物体都拥有修复由损伤因子在其DNA中产生的双链断裂(dsb)的机制。在V(D)J重组过程中也会引入位点特异性dsb。四组对辐射敏感的啮齿动物突变体在dsb修复方面存在缺陷,并且无法有效地进行V(D)J重组。严重联合免疫缺陷(scid)小鼠的免疫缺陷也源于无法进行有效的V(D)J重组,scid细胞系表现出修复缺陷并且属于这些互补组之一。这些发现表明DNA修复和V(D)J重组过程之间存在机制重叠。最近,由这些互补组定义的两个基因已被鉴定出来,并显示编码DNA依赖性蛋白激酶(DNA-PK)的组分。我们在此回顾因这些发现而联系起来的三个领域,并讨论DNA-PK在dsb重新连接和V(D)J重组中的作用。