Abstract
The study of the genetic basis of the manifestation of radiation-induced effects and their transgenerational inheritance makes it possible to identify the mechanisms of adaptation and possible effective strategies for the survival of organisms in response to chronic radioactive stress. One persistent hypothesis is that the activation of certain genes involved in cellular defense is a specific response of the cell to irradiation. There is also data indicating the important role of transposable elements in the formation of radiosensitivity/radioresistance of biological systems. In this work, we studied the interaction of the systems of hobo transposon activity and DNA repair in the cell under conditions of chronic low-dose irradiation and its participation in the inheritance of radiation-induced transgenerational instability in Drosophila. Our results showed a significant increase of sterility and locus-specific mutability, a decrease of survival, fertility and genome stability (an increase the frequency of dominant lethal mutations and DNA damage) in non-irradiated F1/F2 offspring of irradiated parents with dysfunction of the mus304 gene which is responsible for excision and post-replicative recombination repair and repair of double-stranded DNA breaks. The combined action of dysfunction of the mus309 gene and transpositional activity of hobo elements also led to the transgenerational effects of irradiation but only in the F1 offspring. Dysfunction of the genes of other DNA repair systems (mus101 and mus210) showed no visible effects inherited from irradiated parents subjected to hobo transpositions. The mei-41 gene showed specificity in this type of interaction, which consists in its higher efficiency in sensing events induced by transpositional activity rather than irradiation.
Highlights
Ionizing radiation induces biological and genetic effects that have been the subject of detailed study for many years
Our results showed a significant increase of sterility and locus-specific mutability, a decrease of survival, fertility and genome stability in non-irradiated F1/F2 offspring of irradiated parents with dysfunction of the mus304 gene which is responsible for excision and post-replicative recombination repair and repair of double-stranded DNA breaks
One of the most important cellular systems responding to irradiation is the DNA repair system which is actively involved in the elimination of DNA damages even before they turn into mutational events (Bregliano et al, 1995)
Summary
Ionizing radiation induces biological and genetic effects that have been the subject of detailed study for many years. When the cell is irradiated, an increased activity of transposable elements (TEs) associated with stress resistance genes, in particular, DNA repair genes, Transgenerational Effects of Irradiation in Drosophila Melanogaster is observed. As a result of such crosses, inactive transposons (P and hobo) of males of strong P and H strains become active after crossing with females of M and E strains which lack the repressor protein of transposition (Kidwell et al, 1977; Bazin and Higuet, 1996). Entering the cytoplasm lacking the repressor protein of transposition, P and hobo elements encode the enzyme (transposase) of their own transposition which lead to DNA damage and genetic breakdowns (Bazin et al, 1999). Unlike other TEs (retrotransposons that move by the “copy-paste” mechanism and do not break the integrity of the DNA structure), transposons are able to move through the genome using the “cut-paste” mechanism and lead to the formation of double-stranded DNA breaks (DSBs) (Sobels and Eeken, 1981; Finnegan, 1989; Kaufman and Rio, 1992)
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