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Human PDE3A regulates the expression of anti-oxidant genes by controlling Yap1p oxidation in yeast

Wednesday, November 06, 2013 — Poster Session I

4:00 p.m. – 6:00 p.m.

FAES Academic Center (Upper-Level Terrace)




  • DK Rhee
  • JC Lim
  • S Hockman
  • F Ahmad
  • S Liu
  • A Hockman
  • V Manganiello


For overcoming environmental stress via protective antioxidant activity, stress responses mainly entail the transcriptional activation of genes encoding defense and repair proteins. Yeast Yap1p is required for the transcriptional response to oxidative stress, is a sensor of the redox-state, and is a bZIP-containing factor similar to the mammalian AP-1 transcription factor complex. Under oxidative stress, activation of Yap1p is coincident with oxidation of Yap1p and nuclear localization. H2O2 treatment is also thought to increase phosphorylation of Yap1p. However, it is unknown which kinase is responsible for the function of Yap1p. cAMP/PKA signaling pathways are related to increased resistance to H2O2. PDEs control cAMP pools that are components of the RAS/cAMP pathway that regulates general stress responses. Here, we studied the effects of expressed WT hPDE3A and an ubiquitinylation site mutant K13R hPDE3A on H2O2-mediated stress responses, using yeast as a model system. Our results suggest that hPDE3A regulates YAP1-dependent antioxidant genes expression in an ubiquitinylation dependent manner, which in turn leads to increased or decreased expression of cellular target genes involved in recovery from oxidative stress, including regulation of the thioredoxin system. We also show that the oxidation of Yap1p might be regulated by hPDE3A in an ubiquitinylation dependent manner.

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