Lauriston Taylor lecture. 70 years of radiation genetics: fruit flies, mice and humans.
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Recent knowledge of UV-resistance mechanisms in microorganisms is reviewed in perspective, with emphasis on E. coli. Dark-repair genes are classified into "excision" and "tolerance" (ability to produce a normal copy of DNA from damaged DNA). The phenotype of DNA repair is rather common among the microorganisms compared, and yet their molecular mechanisms are not universal. In contrast, DNA photoreactivation is the simplest and the most general among these three repair systems. It is proposed that DNA repair mechanisms evolved in the order: photoreactivation, excision repair, and tolerance repair. The UV protective capacity and light-inducible RNA photoreactivation possessed by some plant viruses are interpreted to be the result of solar UV selection during a rather recent era of evolution.
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In recent years, a substantial amount of information has been obtained on the molecular nature of spontaneous mutations underlying human mendelian diseases, and on the mechanisms that give rise to these mutations. These data, when considered together with data on mutations induced by ionizing radiation in mammalian experimental systems, support the view that current radiation risk estimates for mendelian diseases (which are based on mouse data) are conservative.
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The study concerned antiradiation effects in germ-cell genetic structures produced by a combination of ATP, AET, and serotonin at dose ratio optimal for lethality namely, 45:3:1, as arrived at in our previous work. Such a combination was found to reduce by a factor of 2 the translocation yields observed after 400 R X-rays to mouse spermatogonia. In terms of animal survival, ATP has been shown to contribute little to total protection achieved by the same combination; in terms of genetic damage; however, the role of ATP proved essential. Removal of ATP from the combination led to a significant reduction in protective effect.
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