College of Life Sciences, Capital Normal University, Beijing 100048, China.
FEBS Lett. 2011 Sep 16;585(18):2786-94. doi: 10.1016/j.febslet.2011.04.044. Epub 2011 Apr 28.
Living organisms not only repair DNA damage induced by environmental agents and endogenous cellular metabolites, but have also developed mechanisms to survive in the presence of otherwise lethal lesions. DNA-damage tolerance (DDT) is considered such a mechanism that resumes DNA synthesis in the presence of replication-blocking lesions. Recent studies revealed that DDT in budding yeast is achieved through sequential ubiquitination of DNA polymerase processivity factor, proliferating cell nuclear antigen (PCNA). It is generally believed that monoubiquitinated PCNA promotes translesion DNA synthesis, whereas polyubiquitinated PCNA mediates an error-free mode of lesion bypass. This review will discuss how ubiquitinated PCNA modulates different means of lesion bypass.
生物体不仅能修复环境因素和内源性细胞代谢物引起的 DNA 损伤，还进化出了在存在潜在致死性损伤的情况下存活的机制。DNA 损伤容忍（DDT）被认为是一种能在复制受阻的损伤存在的情况下恢复 DNA 合成的机制。最近的研究表明，在 budding 酵母中，DDT 是通过 DNA 聚合酶持续因子、增殖细胞核抗原（PCNA）的顺序泛素化来实现的。人们普遍认为，单泛素化的 PCNA 促进跨损伤 DNA 合成，而多泛素化的 PCNA 则介导无差错的损伤绕过模式。这篇综述将讨论泛素化的 PCNA 如何调节不同的损伤绕过方式。
