On the nature of interactions leading to radiation-induced chromosomal exchange

Research output: Contribution to journalArticle

13 Citations (Scopus)

Abstract

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.

Original languageEnglish (US)
Pages (from-to)635-643
Number of pages9
JournalInternational Journal of Radiation Biology
Volume56
Issue number5
DOIs
StatePublished - 1989
Externally publishedYes

Fingerprint

chromosomes
Chromosomes
telomeres
lesions (animal)
lesions
Radiation
Telomere
giant cells
Giant Cells
radiation
Fusion reactions
fusion
cells
interactions
damage
mitosis
chromatin
Cell Fusion
genome
DNA probes

ASJC Scopus subject areas

  • Radiology Nuclear Medicine and imaging
  • Radiological and Ultrasound Technology
  • Agricultural and Biological Sciences (miscellaneous)
  • Nuclear Energy and Engineering
  • Radiation

Cite this

On the nature of interactions leading to radiation-induced chromosomal exchange. / Cornforth, Michael.

In: International Journal of Radiation Biology, Vol. 56, No. 5, 1989, p. 635-643.

Research output: Contribution to journalArticle

@article{884ae9bbbe8d447688dda7271f6f6828,
title = "On the nature of interactions leading to radiation-induced chromosomal exchange",
abstract = "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.",
author = "Michael Cornforth",
year = "1989",
doi = "10.1080/09553008914551851",
language = "English (US)",
volume = "56",
pages = "635--643",
journal = "International Journal of Radiation Biology",
issn = "0955-3002",
publisher = "Informa Healthcare",
number = "5",

}

TY - JOUR

T1 - On the nature of interactions leading to radiation-induced chromosomal exchange

AU - Cornforth, Michael

PY - 1989

Y1 - 1989

N2 - 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.

AB - 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.

UR - http://www.scopus.com/inward/record.url?scp=0024367428&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=0024367428&partnerID=8YFLogxK

U2 - 10.1080/09553008914551851

DO - 10.1080/09553008914551851

M3 - Article

VL - 56

SP - 635

EP - 643

JO - International Journal of Radiation Biology

JF - International Journal of Radiation Biology

SN - 0955-3002

IS - 5

ER -