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分裂后期染色质桥与TMP + UVA(365纳米)诱导的CHO细胞染色体畸变之间的关系。

Relationship between chromatin bridges in anaphase and chromosomal aberrations induced by TMP + UVA (365 nm) in CHO cells.

作者信息

Botta R, Gustavino B

机构信息

Dipartimento di Biologia, Università di Roma Tor Vergata, Italy.

出版信息

Mutat Res. 1997 Mar 21;374(2):253-9. doi: 10.1016/s0027-5107(96)00240-0.

DOI:10.1016/s0027-5107(96)00240-0
PMID:9100848
Abstract

In a recent paper, the hypothesis of 'conservative pairing' between complementary DNA strands belonging to both sister chromatids has been proposed as a phenomenon that could account for, at least in part, sister chromatid pairing in late G2/mitosis. The hypothesis was verified through a cytogenetic approach, studying the so-called 'sister chromatid chromatin bridges' (SCCBs), induced in the previous G2/mitosis by a crosslinking (TMP + UVA 365 nm) treatment in CHO cells (Rizzoni, M., E. Cundari, P. Perticone and B. Gustavino (1993) Chromatin bridges between sister chromatids induced in late G2 mitosis in CHO cells by trimethylpsoralen + UVA. Experimental Cell Res., 209, 149-155; [1]). The purpose of the present paper is the study of the relationship between chromatin bridges without fragments in ana-telophase, which were demonstrated to be SCCBs, and chromosomal aberrations, in order to investigate their mechanism of induction. The evolution along the time of the two classes of mitotic anomalies was studied and a comparison was carried out to verify whether the bridges rise as a direct and immediate effect of the treatment or represent the misrepair-mediated effect of it. The present data show that single bridges without fragments come from a direct effect of photoinduced crosslinks in late G2/mitosis. Moreover TMP + 365 nm UVA treatment shows an S-dependent clastogenic effect. The proposed hypothesis of 'conservative pairing' between DNA strands of sister chromatids is further supported.

摘要

在最近的一篇论文中,有人提出属于两条姐妹染色单体的互补DNA链之间存在“保守配对”假说,认为这种现象至少可以部分解释G2晚期/有丝分裂期的姐妹染色单体配对。该假说通过细胞遗传学方法得到验证,研究对象是在之前的G2/有丝分裂期由交联(三甲基补骨脂素+365nm紫外线A)处理诱导产生的所谓“姐妹染色单体染色质桥”(SCCBs)(里佐尼,M.,E. 昆达里,P. 佩尔蒂科内和B. 古斯塔维诺(1993年)三甲基补骨脂素+紫外线A在CHO细胞G2晚期有丝分裂期诱导产生的姐妹染色单体之间的染色质桥。《实验细胞研究》,209,149 - 155;[1])。本文的目的是研究后期/末期无片段的染色质桥(已证明是SCCBs)与染色体畸变之间的关系,以探究它们的诱导机制。研究了这两类有丝分裂异常随时间的演变,并进行了比较,以验证这些桥是作为处理的直接即时效应出现,还是代表其错配修复介导的效应。目前的数据表明,无片段的单个桥来自G2晚期/有丝分裂期光诱导交联的直接效应。此外,三甲基补骨脂素+365nm紫外线A处理显示出依赖于S期的致断裂效应。姐妹染色单体DNA链之间“保守配对”的提出假说得到了进一步支持。

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