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Updated: Aug 8, 2026
Growth-based Determination and Biochemical Confirmation of Genetic Requirements for Protein Degradation in Saccharomyces cerevisiae
Published on: February 16, 2015
Old yellow enzyme interferes with Bax-induced NADPH loss and lipid peroxidation in yeast
Rieka Reekmans1, Kris De Smet, Cuiying Chen
1Unit of Fundamental and Applied Molecular Biology, Department for Molecular Biomedical Research, VIB-Ghent University, Technologiepark 927, B-9052 Zwijnaarde, Belgium.
Abstract:
The yeast transcriptional response to murine Bax expression was compared with the changes induced by H(2)O(2) treatment via microarray technology. Although most of the Bax-responsive genes were also triggered by H(2)O(2) treatment, OYE3, ICY2, MLS1 and BTN2 were validated to have a Bax-specific transcriptional response not shared with the oxidative stress trigger. In knockout experiments, only deletion of OYE3, coding for yeast Old yellow enzyme, attenuated the rate of Bax-induced growth arrest, cell death and NADPH decrease. Lipid peroxidation was completely absent in DeltaOYE3 expressing Bax. However, the absence of OYE3 sensitized yeast cells to H(2)O(2)-induced cell death, and increased the rate of NADPH decrease and lipid peroxidation. Our results clearly indicate that OYE3 interferes with Bax- and H(2)O(2)-induced lipid peroxidation and cell death in Saccharomyces cerevisiae.
Insights
The Old yellow enzyme (OYE3) in yeast plays a dual role in cell death and lipid peroxidation, influencing responses to both Bax protein and hydrogen peroxide (H2O2). OYE3 specifically impacts Bax-induced cell death but not H2O2-induced death.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Murine Bax protein induces cell death in yeast.
- Oxidative stress, exemplified by hydrogen peroxide (H2O2), also triggers cellular responses.
- Understanding the interplay between apoptosis-inducing proteins and oxidative stress is crucial.
Purpose of the Study:
- To compare the yeast transcriptional response to murine Bax expression versus H2O2 treatment.
- To identify genes with specific transcriptional responses to Bax.
- To elucidate the role of specific genes, particularly OYE3, in Bax- and H2O2-induced cellular damage.
Main Methods:
- Microarray technology was employed to analyze global gene expression changes.
- Gene knockout experiments were performed to assess the function of specific genes (e.g., OYE3).
- Measurements included growth arrest, cell death rates, NADPH levels, and lipid peroxidation.
Main Results:
- Most Bax-responsive genes were also induced by H2O2, but OYE3, ICY2, MLS1, and BTN2 showed Bax-specific responses.
- Deletion of OYE3 (DeltaOYE3) attenuated Bax-induced growth arrest, cell death, and NADPH decrease.
- OYE3 deletion prevented Bax-induced lipid peroxidation but sensitized cells to H2O2-induced death and increased NADPH decrease and lipid peroxidation.
Conclusions:
- OYE3 plays a significant role in modulating lipid peroxidation and cell death in Saccharomyces cerevisiae.
- OYE3's function is distinct in Bax- and H2O2-mediated cellular damage pathways.
- OYE3 acts as a key regulator in the cellular defense against Bax-induced toxicity and influences oxidative stress responses.
