On the nature of interactions leading to radiation-induced chromosomal exchange.
On the nature of interactions leading to radiation-induced chromosomal exchange.
复制标题
关于导致辐射诱导染色体交换的相互作用的本质。
DOI：
10.1080/09553008914551851
复制
发表时间：
1989
影响因子：
2.6
通讯作者：
Cornforth,MN
中科院分区：
文献类型：
--
作者：
Cornforth,MN
Within the conceptual framework of so-called lesion-interaction models, chromosomal interchanges are believed to result from radiation damage to both chromosomes involved. More recently, models of radiation action have been proposed which suggest such exchanges arise from initial damage to only one chromosome, which then associates with an undamaged chromosome. The specific case of ‘lesion—nonlesion’ chromosomal interaction via telomere-break rejoining was examined through the use of a telomere-specific DNA probe. No evidence was found to support dicentric formation by this mechanism in normal human fibroblasts. To test the more general case (i.e. lesion—nonlesion interaction by some other mechanism) mitotic HeLa cells were fused together to determine whether exchanges would occur between the chromosomes of previously separate genomes, as seen in resulting cell syncytia at the next mitosis. The fusion of irradiated cells (with each other) produced a high frequency of such intergenomic exchanges. However, the frequency of these events was reduced 50–100-fold in syncytia resulting from the fusion of irradiated with unirradiated cells. These results strongly support the view that most radiation-induced exchange aberrations require initial damage to chromatin at both locations involved in the exchange—i.e. they are fundamentally two-hit in nature.
