Tsukamoto Y, Ikeda H
Department of Molecular Biology, Institute of Medical Science, University of Tokyo, Japan.
Genes Cells. 1998 Mar;3(3):135-44. doi: 10.1046/j.1365-2443.1998.00180.x.
DNA double-strand breaks formed by ionizing irradiation or other stresses are repaired by homologous recombination or DNA end-joining. This review focuses on the mechanism of double-strand break repair mediated by DNA end-joining, in which many factors have recently been identified. After DNA double-strand breakage, DNA end-joining takes place between the DNA ends that have nonhomologous sequences or very short regions ofhomology. The broken DNA is repaired if the DNA end-joining occurs in the same molecule, while it causes chromosome aberrations such as deletions, insertions, translocations and inversions if it occurs between different molecules. Rad50 and its relatives, Ku-proteins, DNA ligase VI and silencing factors, are involved in DNA end-joining in yeast and mammalian cells. These findings led us to propose a model in which the formation of a heterochromatin-like complex at broken ends is an important element in DNA end-joining.
由电离辐射或其他应激形成的DNA双链断裂通过同源重组或DNA末端连接进行修复。本综述聚焦于由DNA末端连接介导的双链断裂修复机制，最近已鉴定出许多相关因子。DNA双链断裂后，DNA末端连接发生在具有非同源序列或非常短同源区域的DNA末端之间。如果DNA末端连接发生在同一分子中，断裂的DNA会被修复；而如果发生在不同分子之间，则会导致染色体畸变，如缺失、插入、易位和倒位。Rad50及其相关蛋白、Ku蛋白、DNA连接酶VI和沉默因子参与酵母和哺乳动物细胞中的DNA末端连接。这些发现使我们提出一个模型，即在断裂末端形成异染色质样复合物是DNA末端连接的一个重要因素。
