Postreplication repair: questions of its definition and possible alteration in xeroderma pigmentosum cell strains.

Postreplication repair: questions of its definition and possible alteration in xeroderma pigmentosum cell strains.
复制标题

复制后修复:其定义和着色性干皮病细胞株中可能的改变的问题。

DOI:
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复制
发表时间:
1979
影响因子:
11.1
通讯作者:
J. Cleaver
J. Cleaver
中科院分区:
综合性期刊1区
文献类型:
--
作者:
S. Park;J. Cleaver

文献摘要

被引文献

相似文献

用紫外线照射正常细胞、切除缺陷细胞和变异着色性干皮病细胞,观察其DNA合成的变化。在照射后1-2小时的[3 H]胸苷的短暂脉冲期间合成的DNA的大小减少,着色性干皮病变体显示出最小的分子量。然而,一旦合成,在所有细胞株中,标记的DNA在与对照相同的大鼠中大小增加,并且该速率对咖啡因相对不敏感。2-3小时后,每种细胞类型中的标记DNA达到最大尺寸,其小于对照细胞中的最大尺寸,表明存在DNA链生长的长寿命阻断物。这种实验(脉冲追踪)过去曾被用来研究一种修复过程,这种修复过程被认为与亲本DNA中受损位点的旁路有关:复制后修复。我们提出了一种替代模型,不涉及一个特定的postreplication修复机制,但涉及一个特定的postreplication修复机制,但涉及正常的链延长和终止机制,我们认为,二聚体和其他受损的网站作为好或没有块复制叉的进展。没有证据可以发现任何诱导过程,增强了受损部位的旁路。
DNA synthesis in normal cells and in excision-defective and variant xeroderma pigmentosum cells was investigated after irradiation with ultraviolet light. The sizes of DNA synthesized during brief pulses of [3H]thymidine 1-2 hr after irradiation were decreased, the xeroderma pigmentosum variant showing the smallest molecular weight. Once synthesized, however, labeled DNA increased in size at the same rat as control in all cell strains, and the rate was relatively insensitive to caffeine. After 2-3 hr, labeled DNA in each cell type reached a maximum size that was less than that in control cells, indicating the presence of long-lived blocks to DNA chain growth. This kind of experiment (pulse-chase) has in the past been used to investigate a repair process believed to be associated with the bypass of damaged sites in parental DNA: postreplication repair. We present an alternative model that does not involve a specific postreplication repair mechanism, but involve a specific postreplication repair mechanism, but involves normal chain elongation and termination mechanisms in which we conceive that dimers and other damaged sites act as well-or-nothing blocks to the progress of replication forks. No evidence could be found for any inducible process that enhanced the bypass of damaged sites.