RNA interference (RNAi) was performed using double-stranded RNAs (dsRNAs) synthesized from gld-2 cDNAs. Young adults were injected with gld-2 dsRNA or soaked in a solution of gld-2 dsRNA for 12 hours at 20°C. Embryos were collected at defined intervals and processed together. A poly(A) polymerase assay was conducted using in vitro-translated proteins and a scintillation counting method with poly(A) as a substrate. RNA oligo (C35A10) and MgCl2 were used in gel assays. The study also included references to various scientific papers. The Forkhead transcription factor FOXO3a protects quiescent cells from oxidative stress by increasing the expression of manganese superoxide dismutase (MnSOD). This protection is achieved through the direct regulation of MnSOD mRNA and protein levels. In the absence of PKB activity, FOXO3a activation leads to increased MnSOD expression, which protects cells from oxidative stress and apoptosis. The study shows that FOXO3a directly binds to the MnSOD promoter, regulating its expression. FOXO3a-mediated protection is essential for cell survival under glucose deprivation. The study also demonstrates that FOXO3a activation leads to quiescence and that this process is regulated by the PKB-Forkhead pathway. The findings suggest that the PKB-Forkhead system acts as a molecular switch controlling cell proliferation and protection from oxidative stress. The study also highlights the evolutionary conservation of this regulatory system in various organisms.RNA interference (RNAi) was performed using double-stranded RNAs (dsRNAs) synthesized from gld-2 cDNAs. Young adults were injected with gld-2 dsRNA or soaked in a solution of gld-2 dsRNA for 12 hours at 20°C. Embryos were collected at defined intervals and processed together. A poly(A) polymerase assay was conducted using in vitro-translated proteins and a scintillation counting method with poly(A) as a substrate. RNA oligo (C35A10) and MgCl2 were used in gel assays. The study also included references to various scientific papers. The Forkhead transcription factor FOXO3a protects quiescent cells from oxidative stress by increasing the expression of manganese superoxide dismutase (MnSOD). This protection is achieved through the direct regulation of MnSOD mRNA and protein levels. In the absence of PKB activity, FOXO3a activation leads to increased MnSOD expression, which protects cells from oxidative stress and apoptosis. The study shows that FOXO3a directly binds to the MnSOD promoter, regulating its expression. FOXO3a-mediated protection is essential for cell survival under glucose deprivation. The study also demonstrates that FOXO3a activation leads to quiescence and that this process is regulated by the PKB-Forkhead pathway. The findings suggest that the PKB-Forkhead system acts as a molecular switch controlling cell proliferation and protection from oxidative stress. The study also highlights the evolutionary conservation of this regulatory system in various organisms.