Spivak Graciela, Cox Rachel A, Hanawalt Philip C
Department of Biological Sciences, Stanford University, Stanford, CA 94305-5020, USA.
Mutat Res. 2009 Jan-Feb;681(1):44-50. doi: 10.1016/j.mrrev.2007.12.003. Epub 2008 Jan 17.
Transcription-coupled repair (TCR) is a pathway dedicated to the removal of damage from the template strands of actively transcribed genes. Although the detailed mechanism of TCR is not yet understood, it is believed to be triggered when a translocating RNA polymerase is arrested at a lesion or unusual structure in the DNA. Conventional assays for TCR require high doses of DNA damage for the statistical analysis of repair in the individual strands of DNA sequences ranging in size from a few hundred bases to 30kb. The single cell gel electrophoresis (Comet) assay allows detection of single- or double-strand breaks at a 10-100-fold higher level of resolution. Fluorescence in situ hybridization (FISH) combined with the Comet assay (Comet-FISH) affords a heightened level of sensitivity for the assessment of repair in defined DNA sequences of cells treated with physiologically relevant doses of genotoxins. This approach also reveals localized susceptibility to chromosomal breakage in cells from individuals with hypersensitivity to radiation or chemotherapy. Several groups have reported preferential repair in transcriptionally active genes or chromosomal domains using Comet-FISH. The prevailing interpretation of the behavior of DNA in the Comet assay assumes that the DNA is arranged in loops and matrix-attachment sites; that supercoiled, undamaged loops are contained within the nuclear matrix and appear in Comet "heads", and that Comet "tails" consist of relaxed DNA loops containing one or more breaks. According to this model, localization of FISH probes in Comet heads signifies that loops containing the targeted sequences are free of damage. This implies that preferential repair as detected by Comet-FISH might encompass large chromosomal domains containing both transcribed and non-transcribed sequences. We review the existing evidence and discuss the implications in relation to current models for the molecular mechanism of TCR.
转录偶联修复(TCR)是一种专门用于去除活跃转录基因模板链上损伤的途径。尽管TCR的详细机制尚未完全明了,但据信当一个正在移位的RNA聚合酶在DNA损伤处或异常结构处停滞时会触发该过程。传统的TCR检测需要高剂量的DNA损伤,以便对大小从几百个碱基到30kb不等的DNA序列单链中的修复进行统计分析。单细胞凝胶电泳(彗星)检测能够以高10 - 100倍的分辨率检测单链或双链断裂。荧光原位杂交(FISH)与彗星检测相结合(彗星-FISH),对于评估用生理相关剂量的基因毒素处理的细胞中特定DNA序列的修复具有更高的灵敏度。这种方法还揭示了对辐射或化疗过敏个体的细胞中染色体断裂的局部易感性。几个研究小组已经报道了使用彗星-FISH在转录活性基因或染色体区域中的优先修复。彗星检测中DNA行为的主流解释假定DNA以环和基质附着位点的形式排列;超螺旋、未受损的环包含在核基质中并出现在彗星“头部”,而彗星“尾部”由包含一个或多个断裂的松弛DNA环组成。根据这个模型,FISH探针在彗星头部的定位表明包含目标序列的环没有损伤。这意味着彗星-FISH检测到的优先修复可能涵盖包含转录和非转录序列的大染色体区域。我们回顾了现有证据,并讨论了其与当前TCR分子机制模型的相关性。