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紫外线和电离辐射通过诱导一种移动DNA元件(L1Rn)的反转录转座,导致大鼠氯白血病细胞程序性死亡。

UV light and ionizing radiations cause programmed death of rat chloroleukaemia cells by inducing retropositions of a mobile DNA element (L1Rn).

作者信息

Servomaa K, Rytömaa T

机构信息

Laboratory of Radiobiology, Finnish Centre for Radiation and Nuclear Safety, Helsinki.

出版信息

Int J Radiat Biol. 1990 Feb;57(2):331-43. doi: 10.1080/09553009014552441.

DOI:10.1080/09553009014552441
PMID:1968498
Abstract

The long interspersed repetitive DNA, L1 or LINE, is a class of mobile genetic elements which can amplify in the cell genome by retroposition, i.e. by a mechanism similar to that of retroviruses. We have shown before that in rat chloroleukaemia cells, maintained in suspension culture in vitro, this element is spontaneously transcriptionally activated at about half of the maximal population density. About 24 h later an explosive amplification of the L1 element is seen in DNA: about 300,000 copies are inserted into apparently random locations in the cell genome, thus creating an outburst of lethal mutations. Dead cells display morphological features typical to programmed death. The present results show that UV light and ionizing radiation induce rapid, premature activation of the L1Rn element during the fast exponential growth of chloroleukaemia cells, and that also this exogenously induced activation is followed by programmed cell death. Transcriptional activation of the L1Rn element can be very strong after the UV exposure: at least 70-fold. Severe hyperthermia, lethal to the cells, does not lead to L1Rn activation (actually a marked suppression is seen) and the mode of phenomic death is necrosis. Some biological implications of the results are discussed.

摘要

长散在重复DNA,即L1或LINE,是一类可通过逆转座作用(即类似于逆转录病毒的机制)在细胞基因组中扩增的移动遗传元件。我们之前已经表明,在体外悬浮培养的大鼠氯白血病细胞中,该元件在最大群体密度的大约一半时会自发地被转录激活。大约24小时后,在DNA中可见L1元件的爆发性扩增:约300,000个拷贝被插入到细胞基因组中明显随机的位置,从而引发致死性突变的爆发。死亡细胞呈现出典型的程序性死亡形态特征。目前的结果表明,紫外线和电离辐射在氯白血病细胞快速指数生长期间诱导L1Rn元件快速、过早激活,并且这种外源性诱导的激活之后也会发生程序性细胞死亡。紫外线照射后L1Rn元件的转录激活可能非常强烈:至少70倍。对细胞致死的严重热疗不会导致L1Rn激活(实际上会出现明显的抑制),且细胞死亡模式为坏死。讨论了这些结果的一些生物学意义。

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UV light and ionizing radiations cause programmed death of rat chloroleukaemia cells by inducing retropositions of a mobile DNA element (L1Rn).紫外线和电离辐射通过诱导一种移动DNA元件(L1Rn)的反转录转座,导致大鼠氯白血病细胞程序性死亡。
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