Collins A, Waldren C
J Cell Sci. 1982 Oct;57:261-75. doi: 10.1242/jcs.57.1.261.
UV-I, an ultraviolet-sensitive mutant of CHO-KI, is abnormally slow to recover from the inhibition of DNA synthesis caused by u.v. irradiation. When synchronized UV-I cells are irradiated in G1, their movement into S phase is unaltered, but thymidine incorporation is depressed (compared with that in the parent cell similarly treated). When irradiated in S phase, again incorporation is more depressed, and S phase suffers a greater delay in UV-I than in the parent cell. UV-I and its parent have similar capacities for excision repair of u.v.-induced damage inflicted in G1, and so enter S phase with similar amounts of unrepaired damage. The single-cell survival was measured after irradiation at different points in the cell cycle. The mutant and parent cells have similar values of D0 (mean lethal dose) except in mitosis, when the parent cell shows markedly greater resistance to u.v. irradiation. Dq (quasi-threshold dose) is fairly constant for the parent cell, but in UV-I it falls to a minimum in S phase. The responses of UV-I to u.v. irradiation are generally consistent with its known defect in the process of post-replication recovery, i.e. the ability to join up the abnormally small DNA fragments synthesized on a u.v.-damaged template.
UV-I是中国仓鼠卵巢细胞系(CHO-K1)的一种紫外线敏感突变体,在紫外线照射引起的DNA合成抑制后,其恢复速度异常缓慢。当处于同步化状态的UV-I细胞在G1期受到照射时,它们进入S期的进程未受影响,但胸苷掺入量降低(与同样处理的亲本细胞相比)。当在S期受到照射时,胸苷掺入量再次受到更大程度的抑制,并且与亲本细胞相比,UV-I细胞的S期延迟更明显。UV-I及其亲本对于G1期紫外线诱导损伤的切除修复能力相似,因此进入S期时未修复损伤的量也相似。在细胞周期的不同时间点进行照射后,测定单细胞存活率。除了在有丝分裂期,亲本细胞对紫外线照射的抗性明显更强外,突变体和亲本细胞的D0(平均致死剂量)值相似。亲本细胞的Dq(准阈值剂量)相当恒定,但在UV-I细胞中,它在S期降至最低。UV-I对紫外线照射的反应总体上与其在复制后恢复过程中已知的缺陷一致,即在紫外线损伤模板上合成的异常小的DNA片段连接能力。