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DNA repair declines with age and correlates with longevity in many animal species. In this study, we investigated the effects of  GAL4 -induced overexpression of genes implicated in DNA repair on lifespan and resistance to stress factors in  Drosophila melanogaster.  Stress factors included hyperthermia, oxidative stress, and starvation. Overexpression was either constitutive or conditional and either ubiquitous or tissue-specific (nervous system). Overexpressed genes included those involved in recognition of DNA damage (homologs of  HUS1, CHK2 ), nucleotide and base excision repair (homologs of  XPF, XPC  and AP-endonuclease-1), and repair of double-stranded DNA breaks (homologs of  BRCA2, XRCC3, KU80  and  WRNexo ). The overexpression of different DNA repair genes led to both positive and negative effects on lifespan and stress resistance. Effects were dependent on  GAL4  driver, stage of induction, sex, and role of the gene in the DNA repair process. While the constitutive/neuron-specific and conditional/ubiquitous overexpression of DNA repair genes negatively impacted lifespan and stress resistance, the constitutive/ubiquitous and conditional/neuron-specific overexpression of  Hus1, mnk, mei-9, mus210 , and  WRNexo  had beneficial effects. This study demonstrates for the first time the effects of overexpression of these DNA repair genes on both lifespan and stress resistance in  D. melanogaster .

Lifespan and Stress Resistance in Drosophila with Overexpressed DNA Repair Genes