Amiard Simon, Gallego Maria E, White Charles I
Génétique, Reproduction et Développement, UMR CNRS 6293/U1103 INSERM/Clermont Université, Université Blaise Pascal Aubiére cedex, France.
Front Plant Sci. 2013 Oct 16;4:405. doi: 10.3389/fpls.2013.00405.
Failure to repair DNA double strand breaks (DSB) can lead to chromosomal rearrangements and eventually to cancer or cell death. Radiation and environmental pollutants induce DSB and this is of particular relevance to plants due to their sessile life style. DSB also occur naturally in cells during DNA replication and programmed induction of DSB initiates the meiotic recombination essential for gametogenesis in most eukaryotes. The linear nature of most eukaryotic chromosomes means that each chromosome has two "broken" ends. Chromosome ends, or telomeres, are protected by nucleoprotein caps which avoid their recognition as DSB by the cellular DNA repair machinery. Deprotected telomeres are recognized as DSB and become substrates for recombination leading to chromosome fusions, the "bridge-breakage-fusion" cycle, genome rearrangements and cell death. The importance of repair of DSB and the severity of the consequences of their misrepair have led to the presence of multiple, robust mechanisms for their detection and repair. After a brief overview of DSB repair pathways to set the context, we present here an update of current understanding of the detection and signaling of DSB in the plant, Arabidopsis thaliana.
未能修复DNA双链断裂（DSB）会导致染色体重排，并最终引发癌症或细胞死亡。辐射和环境污染物会诱导DSB的产生，鉴于植物固着的生活方式，这对植物尤为重要。DSB在DNA复制过程中也会自然发生在细胞中，并且在大多数真核生物中，DSB的程序性诱导启动了配子发生所必需的减数分裂重组。大多数真核生物染色体的线性特征意味着每条染色体都有两个“断裂”末端。染色体末端，即端粒，由核蛋白帽保护，从而避免细胞DNA修复机制将其识别为DSB。脱保护的端粒被识别为DSB，并成为重组的底物，导致染色体融合、“桥-断裂-融合”循环、基因组重排和细胞死亡。DSB修复的重要性以及错误修复后果的严重性导致了多种强大的检测和修复机制的存在。在简要概述DSB修复途径以设定背景之后，我们在此介绍了当前对植物拟南芥中DSB的检测和信号传导的理解更新。
