DNA Damage Checkpoint Response in Plants

尽管在植物中已经发现了一些编码细胞周期直接调节因子的基因，但实际上对于DNA损伤是否会导致细胞周期阻滞在植物中发生一无所知。然而，DNA损伤剂对植物生长有一些有趣的影响，这表明细胞周期阻滞正在发生。当植物像种子一样受到非常高水平的伽马辐射时，种子存活下来，以正常的速度发芽，在环境中正常发育，但不产生任何新细胞。所有的生长都是通过细胞扩增完成的，一株只拥有胚胎叶片的植物被称为“伽玛苗”。已经获得了DNA修复缺陷的突变体，这些突变体对γ辐射诱导的γ -植物效应非常敏感。研究人员将寻找检测DNA损伤持续性并将该信息传递给细胞周期直接调节因子所需的基因。更重要的是，将对这一过程中的突变体进行基因筛选。筛选将允许识别这一过程所需的任何基因，这些基因是植物独有的，或者尚未在动物中被识别出来。在DNA修复突变系中获得γ植株表型的第二位点抑制子。为了减少诱导突变的频率，大多数生物已经发展出检测持续DNA损伤的机制，并将这些信息转导给细胞周期的调节因子。这些损伤特异性的“检查点”为细胞提供了时间，在DNA损伤被处理成突变之前修复它。在DNA损伤特异性检查点中有缺陷的细胞对许多DNA损伤剂的毒性作用既超易变又超敏感。

Britt, A.Although some of the genes encoding the direct regulators of the cell cycle have been identified in plants, virtually nothing is known as to whether DNA damage induced cell cycle arrest occurs in plants. However, there are certain interesting effects of DNA damaging agents on plant growth, which suggest that cell cycle arrest is taking place. When plants are treated as seeds with very high levels of gamma radiation, the seed survives, germinates at a normal rate, develops normally in respect to its environment but does not produce any new cells. All growth occurs through cell expansion and a plant that possesses only its embryonic leaves results, a "gamma plantlet". Mutants have been obtained defective in DNA repair that are hypersensitive to the gamma-plantlet inducing effects of gamma radiation. The genes that are required for detecting the persistence of DNA damage and transducing that information to the direct regulators of the cell cycle will be sought. More importantly, a genetic screen for mutants defective in this process will be performed. The screen will allow identification of any genes required for this process which are unique to plants or which have not yet been identified in animals. Second site suppressors of the gamma plantlet phenotype in the DNA repair mutant line will be obtained.In order to reduce the frequency of induction of mutations, most living things have developed mechanisms for the detection of persisting DNA damage and the transduction of this information to the regulators of the cell cycle. These damage-specific "checkpoints" provide the cell with time in which to repair DNA damage before it is processed into a mutation. Cells defective in DNA damage-specific checkpoints are both hypermutable and hypersensitive to the toxic effects of many DNA damaging agents.