Shim Y S, Jang Y K, Lim M S, Lee J S, Seong R H, Hong S H, Park S D
School of Biological Sciences, Seoul National University, Seoul 151-742, Republic of Korea.
Mol Cell Biol. 2000 Dec;20(23):8958-68. doi: 10.1128/MCB.20.23.8958-8968.2000.
The Schizosaccharomyces pombe DNA repair gene rhp51(+) encodes a RecA-like protein with the DNA-dependent ATPase activity required for homologous recombination. The level of the rhp51(+) transcript is increased by a variety of DNA-damaging agents. Its promoter has two cis-acting DNA damage-responsive elements (DREs) responsible for DNA damage inducibility. Here we report identification of Rdp1, which regulates rhp51(+) expression through the DRE of rhp51(+). The protein contains a zinc finger and a polyalanine tract similar to ones previously implicated in DNA binding and transactivation or repression, respectively. In vitro footprinting and competitive binding assays indicate that the core consensus sequences (NGG/TTG/A) of DRE are crucial for the binding of Rdp1. Mutations of both DRE1 and DRE2 affected the damage-induced expression of rhp51(+), indicating that both DREs are required for transcriptional activation. In addition, mutations in the DREs significantly reduced survival rates after exposure to DNA-damaging agents, demonstrating that the damage response of rhp51(+) enhances the cellular repair capacity. Surprisingly, haploid cells containing a complete rdp1 deletion could not be recovered, indicating that rdp1(+) is essential for cell viability and implying the existence of other target genes. Furthermore, the DNA damage-dependent expression of rhp51(+) was significantly reduced in checkpoint mutants, raising the possibility that Rdp1 may mediate damage checkpoint-dependent transcription of rhp51(+).
粟酒裂殖酵母DNA修复基因rhp51(+)编码一种与RecA相似的蛋白,该蛋白具有同源重组所需的依赖DNA的ATP酶活性。多种DNA损伤剂可使rhp51(+)转录本水平升高。其启动子有两个顺式作用的DNA损伤反应元件(DREs),负责DNA损伤诱导。在此,我们报告了Rdp1的鉴定,它通过rhp51(+)的DRE调节rhp51(+)的表达。该蛋白含有一个锌指和一个多聚丙氨酸序列,分别类似于先前涉及DNA结合以及反式激活或抑制的序列。体外足迹法和竞争性结合试验表明,DRE的核心共有序列(NGG/TTG/A)对Rdp1的结合至关重要。DRE1和DRE2的突变均影响rhp51(+)的损伤诱导表达,表明两个DRE均为转录激活所必需。此外,DREs中的突变显著降低了暴露于DNA损伤剂后的存活率,表明rhp51(+)的损伤反应增强了细胞修复能力。令人惊讶的是,无法获得含有完整rdp1缺失的单倍体细胞,这表明rdp1(+)对细胞活力至关重要,并暗示存在其他靶基因。此外,rhp51(+)的DNA损伤依赖性表达在检查点突变体中显著降低,这增加了Rdp1可能介导rhp51(+)的损伤检查点依赖性转录的可能性。