Cisplatin DNA cross-links do not inhibit S-phase and cause only a G2/M arrest in Saccharomyces cerevisiae
Cisplatin DNA cross-links do not inhibit S-phase and cause only a G2/M arrest in Saccharomyces cerevisiae
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DOI：
10.1016/s0921-8777(99)00011-7
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发表时间：
1999-05-14
期刊：
影响因子：
--
通讯作者：
Moses, RE
中科院分区：
文献类型：
--
作者：
Grossmann, KF;Brown, JC;Moses, RE
顺铂（CDDP）已被用作DNA交联剂，以评估是否有一个特定的细胞周期检查点的反应，这种损伤在酿酒酵母（S，酿酒酵母）。流式细胞仪分析显示只有一个G（2）/M检查点，在α-因子阻滞和CDDP治疗后正常从G（1）退出并进展到S期。在测试的检查点突变体中，与同基因野生型细胞相比，rad 9、rad 17和rad 24没有显示出对CDDP的敏感性增加。然而，检测的其他检查点突变体（mec 1、mec 3和rad 53）显示对CDDP的敏感性增加，切除修复缺陷（rad 1和rad 14）或重组缺陷（rad 51和rad 52）的对照也是如此。因此，通过存活和细胞周期动力学，似乎DNA交联不抑制进入S期或减慢DNA复制，并且在酵母中顺铂处理后复制继续。(C)1999 Elsevier Science B. V.保留所有权利。
Cisplatin (CDDP) has been used as a DNA cross-linking agent to evaluate whether there is a specific cell cycle checkpoint response to such damage in Saccharomyces cerevisiae (S, cerevisiae). Fluorescent-activate cell sorting (FACS) analysis showed only a G(2)/M checkpoint, normal exit from G(1) and progression through S-phase following alpha-factor arrest and CDDP treatment. Of the checkpoint mutants tested, rad9, rad17 and rad24, did not show increased sensitivity to CDDP compared to isogenic wild-type cells. However, other checkpoint mutants tested (mec1, mec3 and rad53) showed increased sensitivity to CDDP, as did controls with a defect in excision repair (rad1 and rad14) or a defect in recombination (rad51 and rad52). Thus, by survival and cell cycle kinetics, it appears that DNA cross-links do not inhibit entry into S-phase or slow DNA replication and that replication continues after cisplatin treatment in yeast. (C) 1999 Elsevier Science B.V. All rights reserved.