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首页> 外文期刊>Cancer radiotherapie: journal de la Soci閠?fran鏰ise de radiotherapie oncologique >Double Strand Break Repair, one mechanism can hide another: Alternative non-homologous end joining [Réparation des cassures double-brin de l'ADN, un mécanisme peut en cacher un autre: La ligature d'extrémités non homologues alternative]
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Double Strand Break Repair, one mechanism can hide another: Alternative non-homologous end joining [Réparation des cassures double-brin de l'ADN, un mécanisme peut en cacher un autre: La ligature d'extrémités non homologues alternative]

机译：双链断裂修复，一种机制可以隐藏另一种：替代性的非同源末端连接[修复DNA中的双链断裂，一种机制可以隐藏另一种：替代性的非同源末端连接]

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DNA double strand breaks are major cytotoxic lesions encountered by the cells. They can be induced by ionizing radiation or endogenous stress and can lead to genetic instability. Two mechanisms compete for the repair of DNA double strand breaks: homologous recombination and non-homologous end joining (NHEJ). Homologous recombination requires DNA sequences homology and is initiated by single strand resection. Recently, advances have been made concerning the major steps and proteins involved in resection. NHEJ, in contrast, does not require sequence homology. The existence of a DNA double strand break repair mechanism, independent of KU and ligase IV, the key proteins of the canonical non homologous end joining pathway, has been revealed lately and named alternative non homologous end joining. The hallmarks of this highly mutagenic pathway are deletions at repair junctions and frequent use of distal microhomologies. This mechanism is also initiated by a single strand resection of the break. The aim of this review is firstly to present recent data on single strand resection, and secondly the alternative NHEJ pathway, including a discussion on the fidelity of NHEJ. Based on current knowledge, canonical NHEJ does not appear as an intrinsically mutagenic mechanism, but in contrast, as a conservative one. The structure of broken DNA ends actually dictates the quality repair of the alternative NHEJ and seems the actual responsible for the mutagenesis attributed beforehand to the canonical NHEJ. The existence of this novel DNA double strand breaks repair mechanism needs to be taken into account in the development of radiosensitizing strategies in order to optimise the efficiency of radiotherapy.
机译：DNA双链断裂是细胞遇到的主要细胞毒性损伤。它们可能是由电离辐射或内源性压力引起的，并可能导致遗传不稳定。两种机制竞争DNA双链断裂的修复：同源重组和非同源末端连接（NHEJ）。同源重组需要DNA序列同源性，并通过单链切除启动。最近，关于切除的主要步骤和蛋白质已经取得了进展。相反，NHEJ不需要序列同源性。 DNA双链断裂修复机制的存在，不依赖于KU和连接酶IV，这是规范性非同源末端连接途径的关键蛋白，最近已被揭示，并被称为替代性非同源末端连接。此高度诱变途径的标志是修复连接处的缺失和远端微同源性的频繁使用。该机制也由断裂的单链切除引发。这篇综述的目的是首先介绍单链切除术的最新数据，其次介绍替代性NHEJ途径，包括有关NHEJ保真度的讨论。根据目前的知识，规范的NHEJ并不是一种固有的诱变机制，相反，它是一种保守的机制。断裂的DNA末端的结构实际上决定了替代NHEJ的质量修复，并且似乎是归因于规范NHEJ事先引起的诱变的实际原因。为了优化放射治疗的效率，在放射增敏策略的开发中需要考虑这种新颖的DNA双链断裂修复机制的存在。

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