The role of DNA repair genes in radiation-induced adaptive response in Drosophila melanogaster is differential and conditional

DNA damage response signaling pathways and targets for radiotherapy sensitization in cancer

“…During IR treatment, cancer cells evolve personalized DNA damage repair mechanisms against IR insults for survival 66 . The induction of DNA mechanisms required to realize the effects of IR has been referred to as "hormesis" 157 . It has been reported that three different primary pathways evolved to process DSB repair: the HR-based pathway, NHEJ, and alternative end joining (Fig.…”

“…For instance, eurycomalactone, an active quassinoid isolated from Eurycoma longifolia Jack, markedly delayed the repair of radiation-induced DSBs in non-small-cell lung cancer (NSCLC) cells 160 . Koval et al 157 reported that a protective system could be activated among cancer cells in response to IR, leading to increased resistance to subsequent exposure to IR, and moreover, chronic exposure to γ-rays increased the expression of the mus210, mus219, and mus309 genes, even after 56 days, in Canton-S flies. Although the development of genome-wide sequencing techniques has allowed scientists to identify the molecular mechanisms of the radiation-induced adaptive response, including the Notch, tumor growth factor-β, mammalian target of rapamycin, and Wnt signaling pathways, the detailed mechanism of cancer cell defense in IR-induced hormesis remains unclear.…”

Tissue-Specific Knockdown of Genes of the Argonaute Family Modulates Lifespan and Radioresistance in Drosophila Melanogaster

“…These genes belong to the basic signaling pathways of reaction to acute irradiation, and their activation ensures survival under adverse conditions [80,84]. Indeed, in vivo and in vitro studies established that the activity of DNA damage recognition and repair genes is necessary for the normal reaction of cells and an organism to the action of ionizing radiation, the formation of specific responses [36,37,40,41]. Similarly, genes encoding heat shock proteins are activated under acute radiation and provide an adaptive response to stress [38,39,85].…”

“…In addition, changes in the levels of retrotransposons and expression of stress response genes were analyzed to determine the molecular mechanisms involved. It was previously found that genes of antioxidant defense, DNA damage response, and repair play a critical role in both lifespan regulation and the reaction of cells, tissues, and a whole organism to ionizing irradiation [33][34][35][36][37][38][39][40][41]. In addition, genes involved in different mechanisms of proteostasis demonstrate changes during aging and after irradiation as well [38,39,42,43].…”

Low-dose ionizing radiation as a hormetin: experimental observations and therapeutic perspective for age-related disorders

“…An important role of genes encoding heat shock proteins and heat shock factors (Moskalev et al 2009) as well as longevity-associated factors such as FOXO, SIRT1, JNK, ATM, ATR, and p53 (Moskalev et al 2011) in inducing radiation-induced hormetic effects in fruit flies also has been demonstrated. More recently, significant contribution of genes implicated in the nucleotide excision repair (mei-9, mus210, Mus209), base excision repair (Rrp1), DNA double-stranded break repair by homologous recombination (Brca2, spn-B, okr), DNA damage sensing (D-Gadd45, Hus1, mnk), non-homologous end joining (Ku80, WRNexo), as well as Mus309 known to participate in the DNA repair processes has been revealed (Koval et al 2020). In flies with mutations in these genes radiation hormesis was completely absent or appeared to a lesser extent than in wild-type Canton-S strain.…”