DNA Damage Checkpoint Response in Plants

虽然在植物中已经发现了一些编码细胞周期直接调节的基因，但几乎没有人知道DNA损伤是否会导致植物细胞周期停滞。然而，DNA损伤剂对植物生长有某些有趣的影响，这表明细胞周期正在发生停滞。当植物被视为具有非常高水平的伽马辐射的种子时，种子存活，以正常的速度萌发，根据环境正常发育，但不产生任何新的细胞。所有的生长都是通过细胞扩张进行的，一个只拥有胚胎叶片的植物就会产生一个“伽马植株”。已经获得了DNA修复缺陷的突变株，这些突变株对伽马射线诱导的伽马植株效应高度敏感。将寻找检测DNA损伤的持久性并将该信息传递给细胞周期的直接调节器所需的基因。更重要的是，将对在这一过程中有缺陷的突变进行遗传筛查。该筛查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，或者是尚未在动物身上识别的。在DNA修复突变系中将获得伽玛植株表型的第二个位点抑制子。为了减少突变诱导的频率，大多数生物已经开发出检测持续DNA损伤并将这些信息转导到细胞周期调节器的机制。这些特定于损伤的“检查点”为细胞提供了在DNA损伤被处理为突变之前修复损伤的时间。在DNA损伤特异性检查点缺陷的细胞既具有高度易变性，又对许多DNA损伤剂的毒性效应高度敏感。

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.