Department of Biochemistry and Molecular Biology, Southern Illinois University, School of Medicine, Carbondale, Illinois 62901, USA.
J Biol Chem. 2012 Oct 19;287(43):36414-22. doi: 10.1074/jbc.M112.364661. Epub 2012 Aug 21.
Previous studies have demonstrated transcription-coupled nucleotide/base excision repair. We report here for the first time that DNA double-strand break (DSB) repair is also coupled to transcription. We generated a yeast strain by introducing a homing (Ho) endonuclease cut site followed by a nucleotide sequence for multiple Myc epitopes at the 3' end of the coding sequence of a highly active gene, ADH1. This yeast strain also contains the Ho cut site at the nearly silent or poorly active mating type α (MATα) locus and expresses Ho endonuclease under the galactose-inducible GAL1 promoter. Using this strain, DSBs were generated at the ADH1 and MATα loci in galactose-containing growth medium that induced HO expression. Subsequently, yeast cells were transferred to dextrose-containing growth medium to stop HO expression, and the DSB repair was monitored at the ADH1 and MATα loci by PCR, using the primer pairs flanking the Ho cut sites. Our results revealed a faster DSB repair at the highly active ADH1 than that at the nearly silent MATα locus, hence implicating a transcription-coupled DSB repair at the active gene in vivo. Subsequently, we extended this study to another gene, PHO5 (carrying the Ho cut site at its coding sequence), under transcriptionally active and inactive growth conditions. We found a fast DSB repair at the active PHO5 gene in comparison to its inactive state. Collectively, our results demonstrate a preferential DSB repair at the active gene, thus supporting transcription-coupled DSB repair in living cells.
先前的研究已经证明了转录偶联的核苷酸/碱基切除修复。我们首次报道了 DNA 双链断裂 (DSB) 修复也与转录偶联。我们通过在高度活跃基因 ADH1 的编码序列的 3' 端引入同源 (Ho) 内切酶切割位点,随后引入多个 Myc 表位的核苷酸序列,在酵母中生成了一个菌株。该酵母菌株还在近乎沉默或活性差的交配型α (MATα) 基因座中含有 Ho 切割位点,并在半乳糖诱导的 GAL1 启动子下表达 Ho 内切酶。使用该菌株,在含有半乳糖的生长培养基中,在 ADH1 和 MATα 基因座处产生 DSB,该培养基诱导 HO 表达。随后,将酵母细胞转移到含有葡萄糖的生长培养基中,以停止 HO 表达,并使用侧翼 Ho 切割位点的引物对,通过 PCR 监测 ADH1 和 MATα 基因座处的 DSB 修复。我们的结果表明,在高度活跃的 ADH1 基因座处的 DSB 修复速度快于近乎沉默的 MATα 基因座,这表明在体内存在转录偶联的 DSB 修复。随后,我们在转录活跃和不活跃的生长条件下,将该研究扩展到另一个基因 PHO5(在其编码序列中携带 Ho 切割位点)。与非活性状态相比,我们发现活跃的 PHO5 基因处的 DSB 修复速度更快。总之,我们的结果表明,在活跃的基因处优先进行 DSB 修复,从而支持活细胞中的转录偶联 DSB 修复。