Abstract
Effect of a 1000 R dose of hard X-rays, with two different dose-rates viz. 300 and 1000 R/min on somatic crossing over in the X chromosome of Drosophila melanogaster was studied in two different genotypes. Irradiation was given during the first-instar larval stage of the development. In the control crosses the flies carried wild-type autosomes, but in the experimental crosses the 3rd chromosomes carried a DNA double-strand break repair deficient mus309 mutant gene constitution. As expected, the frequency of X-ray-induced somatic crossing over increased in the mutant flies with both dose-rates of irradiation. As also expected, in the control flies irradiation given with the 300 R/min dose-rate caused more somatic crossovers than irradiation given with the 1000 R/ min rate. However, rather unexpectedly, in the experimental flies there was no significant difference in the frequency of somatic crossing over between the two dose-rates of irradiation. The results can be explained by assuming that X-ray-induced somatic crossing over is a two-step event, and that the mechanism which repairs the lesion caused by the irradiation is controlled by the mus309 gene. In the control flies the repairing mechanism is capable to recover if the irradiation is given with a short term high dose-rate, but is not capable to recover if the irradiation is given with a long lasting low dose-rate. However, in the experimental mutant flies the repairing mechanism is only poorly recovered irrespective of the dose-rate.
Highlights
Effect of a 1000 R dose of hard X-rays, with two different dose-rates viz. 300 and 1000 R/min on somatic crossing over in the X chromosome of Drosophila melanogaster was studied in two different genotypes
The results can be explained by assuming that X-ray-induced somatic crossing over is a two-step event, and that the mechanism which repairs the lesion caused by the irradiation is controlled by the mus309 gene
This is in contrast with the observation of Johnson-Schlitz and Engels [22] and McVey et al [24] who found that in mus309 mutants the frequency of spontaneous mitotic crossing over in the germ line of the males was increased by several orders of magnitude
Summary
DNA double-strand breaks (DSBs) are considered the most lethal form of DNA damage. They can result from either endogenous or exogenous sources. Occurring DSBs are generated spontaneously during DNA synthesis when the replication fork encounters a damaged template, and during certain cellular processes. Failure to repair DSBs, or their misrepair, may result in cell death or chromosomal rearrangements, including deletions and translocations or genome instability in general. Two major pathways have evolved to repair DSBs and thereby suppress genomic instability. These are the non-homologous end-joining (NHEJ) pathway and homologous recombination (HR), called homology-directed repair (HDR) pathway [1,2]
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