Yu Sung-Lim, Lee Sung-Keun, Johnson Robert E, Prakash Louise, Prakash Satya
Sealy Center for Molecular Science, University of Texas Medical Branch, Galveston 77555-1061, USA.
Mol Cell Biol. 2003 Jan;23(1):382-8. doi: 10.1128/MCB.23.1.382-388.2003.
Abasic (AP) sites represent one of the most frequently formed lesions in DNA. Here, we examine the consequences of the stalling of RNA polymerase II at AP sites in DNA in Saccharomyces cerevisiae. A severe inhibition of transcription occurs in strains that are defective in the removal of AP sites and that also lack the RAD26 gene, a homolog of the human Cockayne syndrome group B (CSB) gene, and, importantly, a dramatic rise in mutagenesis is incurred in such strains. From the various observations presented here, we infer that the stalling of transcription at AP sites is highly mutagenic.
无碱基（AP）位点是DNA中最常形成的损伤之一。在此，我们研究了酿酒酵母中RNA聚合酶II在DNA中的AP位点处停滞的后果。在AP位点去除存在缺陷且还缺乏RAD26基因（人类科凯恩综合征B组（CSB）基因的同源物）的菌株中，转录受到严重抑制，并且重要的是，这些菌株中诱变率显著升高。从这里呈现的各种观察结果来看，我们推断转录在AP位点处的停滞具有高度致突变性。
