Haber James E
MS029 Rosenstiel Center and Department of Biology, Brandeis University, Waltham, MA 02454-9110, USA.
DNA Repair (Amst). 2006 Sep 8;5(9-10):998-1009. doi: 10.1016/j.dnarep.2006.05.025. Epub 2006 Jun 27.
Much of what we know about the molecular mechanisms of repairing a broken chromosome has come from the analysis of site-specific double-strand breaks (DSBs). Such DSBs can be generated by conditional expression of meganucleases such as HO or I-SceI or by the excision of a DNA transposable element. The synchronous creation of DSBs in nearly all cells of the population has made it possible to observe the progress of recombination by monitoring both the DNA itself and proteins that become associated with the recombining DNA. Both homologous recombination mechanisms and non-homologous end-joining (NHEJ) mechanisms of recombination have been defined by using these approaches. Here I focus on recombination events that lead to alterations of chromosome structure: transpositions, translocations, deletions, DNA fragment capture and other small insertions. These rearrangements can occur from ectopic gene conversions accompanied by crossing-over, break-induced replication, single-strand annealing or non-homologous end-joining.
我们对修复断裂染色体的分子机制的许多了解都来自对位点特异性双链断裂（DSB）的分析。此类双链断裂可通过诸如HO或I-SceI等归巢核酸酶的条件性表达或通过DNA转座元件的切除来产生。在群体中几乎所有细胞中同步产生双链断裂，使得通过监测DNA本身以及与重组DNA相关联的蛋白质来观察重组进程成为可能。通过使用这些方法，已经明确了同源重组机制和非同源末端连接（NHEJ）重组机制。在这里，我重点关注导致染色体结构改变的重组事件：转座、易位、缺失、DNA片段捕获以及其他小插入。这些重排可由伴随交换的异位基因转换、断裂诱导复制、单链退火或非同源末端连接产生。
