Cellular responses to inhibition of DNA replication fork progression at DNA lesions

我们研究了真核细胞如何应对各种DNA损伤，阻止DNA复制叉的进展。我们发现其中一种翻译DNA合成聚合酶，DNA聚合酶η，与其他几种修复蛋白（如错配修复蛋白）相互作用，在某些氨基酸残基上被磷酸化和泛素化，并在紫外线照射下改变细胞内定位。我们证明了模板转换机制不仅在原核生物中起作用，而且在高等真核生物中也起作用。

We studied how eukaryotic cells respond to various DNA damages that prevent the progression of DNA replication fork. We found that one of the translesion DNA synthesis polymerase, DNA polymerase η, interacts with several other repair proteins such as mismatch repair proteins, is phosphorylated and ubiquitinated at certain amino acid residues, and changes the intracellular localization upon UV irradiation. We demonstrated that the template-switching mechanism is operating not only in prokaryotes but also in higher eukaryotes.