Repair of radiation-induced damage to chromosomes: Independence of known DNA dark repair mechanisms

Abstract

Chromosomes contain large amounts of protein in addition to DNA and often appear to be multistranded. Despite this it has been proposed that the repair (restitution) of radiation-induced chromosome breaks and the rejoining that leads to the formation of exchanges takes place by the same processes involved in dark repair of DNA, i.e., it has been suggested that there is base pairing of portions of single DNA strands from double helices and resynthesis using the opposite strand as a template. Experiments with Vicia faba root tip cells, Chinese hamster cells of B14FAF and DON lines in tissue culture, and human leukocytes from normal persons as well as patients with Xeroderma pigmentosum show that X-ray induced breaks can rejoin in all of these systems. Since Vicia, B14FAF Chinese hamster cells, and Xeroderma cells do not exhibit unscheduled DNA synthesis (presumably dark repair) the experiments are interpreted to indicate that the repair of chromosomal damage and the formation of exchanges do not occur by dark repair of DNA. This interpretation is strengthened by X-ray dose fractionation studies in Vicia in which it was found that caffeine (which inhibits dark repair in bacteria) does not effect the joining of chromosome breaks. The repair of UV-induced chromosome breaks also seems to be independent of DNA dark repair mechanisms.