Iyer Ravi R, Pluciennik Anna, Napierala Marek, Wells Robert D
Teva Branded Pharmaceutical Products R&D, Inc., West Chester, Pennsylvania 19380; email:
Annu Rev Biochem. 2015;84:199-226. doi: 10.1146/annurev-biochem-060614-034010. Epub 2015 Jan 2.
DNA mismatch repair is a conserved antimutagenic pathway that maintains genomic stability through rectification of DNA replication errors and attenuation of chromosomal rearrangements. Paradoxically, mutagenic action of mismatch repair has been implicated as a cause of triplet repeat expansions that cause neurological diseases such as Huntington disease and myotonic dystrophy. This mutagenic process requires the mismatch recognition factor MutSβ and the MutLα (and/or possibly MutLγ) endonuclease, and is thought to be triggered by the transient formation of unusual DNA structures within the expanded triplet repeat element. This review summarizes the current knowledge of DNA mismatch repair involvement in triplet repeat expansion, which encompasses in vitro biochemical findings, cellular studies, and various in vivo transgenic animal model experiments. We present current mechanistic hypotheses regarding mismatch repair protein function in mediating triplet repeat expansions and discuss potential therapeutic approaches targeting the mismatch repair pathway.
DNA错配修复是一种保守的抗诱变途径,通过纠正DNA复制错误和减少染色体重排来维持基因组稳定性。矛盾的是,错配修复的诱变作用被认为是导致三联体重复序列扩增的原因,而三联体重复序列扩增会引发诸如亨廷顿病和强直性肌营养不良等神经疾病。这种诱变过程需要错配识别因子MutSβ和MutLα(和/或可能还有MutLγ)核酸内切酶,并且被认为是由扩增的三联体重复元件内异常DNA结构的瞬时形成所触发的。本综述总结了目前关于DNA错配修复参与三联体重复序列扩增的知识,其中包括体外生化研究结果、细胞研究以及各种体内转基因动物模型实验。我们提出了关于错配修复蛋白在介导三联体重复序列扩增中功能的当前机制假说,并讨论了针对错配修复途径的潜在治疗方法。