Members of the RecQ family of helicases are known as the “guardians of the genome” due to their essential roles in DNA repair, replication, and recombination. Mutations in the RecQ helicases, WRN and BLM, cause Werner and Bloom syndrome respectively. These autosomal recessive diseases are characterized by patients’ increased risk of cancer and early onset of aging-related pathologies. Similar to Bloom syndrome patients, Blm mutant flies have shortened lifespans and a higher incidence of tumors, particularly in the gut and ovaries of aged females. We have found that flies mutant in the Drosophila homolog of WRN, WRNexo, also exhibit decreased lifespans and higher tumor incidence compared to age-matched wild type controls. In contrast to Blm mutants, WRNexo flies accumulate tumors in the testes, suggesting tissue-specific mechanisms of these two proteins. WRNexo mutants also exhibit other physiological signs of aging such as degeneration of the flight muscles and decreased locomotor activity. Additionally, we observed that mutant flies have increased antioxidant activity that declines with age, suggesting that the aging phenotypes may be due to increased oxidative damage. We propose that WRNexo and BLM physically interact with one another to protect against physiological signs of aging, which is a hypothesis supported by our recent finding that WRNexo and Blm mutants share similar phenotypes in response to replication stress. To this effect, we are investigating these interactions by performing a co-immunoprecipitation assay using WRNexo transgenic mutants.