School of Chemistry, University of Glasgow, Joseph Black Building, University Avenue, Glasgow, G12 8QQ, UK.
Nat Commun. 2021 Jan 8;12(1):204. doi: 10.1038/s41467-020-20426-3.
Expansions of CAG/CTG trinucleotide repeats in DNA are the cause of at least 17 degenerative human disorders, including Huntington's Disease. Repeat instability is thought to occur via the formation of intrastrand hairpins during replication, repair, recombination, and transcription though relatively little is known about their structure and dynamics. We use single-molecule Förster resonance energy transfer to study DNA three-way junctions (3WJs) containing slip-outs composed of CAG or CTG repeats. 3WJs that only have repeats in the slip-out show two-state behavior, which we attribute to conformational flexibility at the 3WJ branchpoint. When the triplet repeats extend into the adjacent duplex, additional dynamics are observed, which we assign to interconversion of positional isomers. We propose a branchpoint migration model that involves conformational rearrangement, strand exchange, and bulge-loop movement. This migration has implications for how repeat slip-outs are processed by the cellular machinery, disease progression, and their development as drug targets.
DNA 中 CAG/CTG 三核苷酸重复序列的扩展是至少 17 种退行性人类疾病的原因,包括亨廷顿病。重复不稳定性被认为是通过复制、修复、重组和转录过程中形成的链内发夹结构发生的,尽管人们对其结构和动力学知之甚少。我们使用单分子Förster 共振能量转移来研究包含 CAG 或 CTG 重复序列的滑出的 DNA 三链结(3WJ)。仅在滑出中具有重复序列的 3WJ 表现出两态行为,我们将其归因于 3WJ 分支点处的构象灵活性。当三联体重复延伸到相邻的双链体时,会观察到额外的动力学,我们将其归因于位置异构体的相互转换。我们提出了一个分支点迁移模型,该模型涉及构象重排、链交换和凸起环运动。这种迁移对细胞机制如何处理重复滑出、疾病进展以及将其作为药物靶点开发具有影响。