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Published on: November 20, 2021
FSH3 mediated cell death is dependent on NUC1 in Saccharomyces cerevisiae
Ramachandran Gowsalya1, Chidambaram Ravi1, Muthukumar Kannan2
1Department of Biochemistry, School of Life Sciences, Bharathidasan University, Tiruchirappalli - 620 024, Tamil Nadu, India.
Abstract:
Family of Serine Hydrolases (FSH) members FSH1, FSH2 and FSH3 in Saccharomyces cerevisiae share conserved sequences with the human candidate tumor suppressor OVCA2. In this study, hydrogen peroxide (H2O2) exposure increased the expression of both mRNA and protein levels of FSH3 in wild-type (WT) yeast cells. The deletion of FSH3 improved the yeast growth rate under H2O2-induction as compared to WT control cells. The overexpression of FSH3 in WT yeast cells caused an apoptotic phenotype, including accumulation of reaction oxygen species, decreased cell viability and cell death. The double deletions fsh1Δ fsh2Δ, fsh1Δ fsh3Δ and fsh2Δ fsh3Δ displayed increased growth compared to WT cells. However, the overexpression of FSH3 effectively inhibited cell growth in all double deletions. Moreover, the overexpression of FSH3 in cells lacking NUC1 did not cause any growth defect in the presence or absence of H2O2. Our results suggest that FSH3 induced apoptosis of yeast in a NUC1 dependent manner.
Insights
Hydrogen peroxide (H2O2) increases Family of Serine Hydrolases 3 (FSH3) expression in yeast. FSH3 overexpression induces apoptosis, but deletion improves growth, suggesting a role in oxidative stress response.
Area of Science:
- Molecular Biology
- Cell Biology
- Yeast Genetics
Background:
- Family of Serine Hydrolases (FSH) proteins, including FSH1, FSH2, and FSH3 in Saccharomyces cerevisiae, share sequence similarity with the human tumor suppressor OVCA2.
- Oxidative stress, induced by hydrogen peroxide (H2O2), is a critical factor influencing cellular processes and survival.
Purpose of the Study:
- To investigate the role of FSH3 in yeast response to oxidative stress.
- To elucidate the mechanism by which FSH3 affects cell growth and viability under H2O2 exposure.
Main Methods:
- Gene expression analysis (mRNA and protein levels) of FSH3 under H2O2 treatment in wild-type (WT) yeast.
- Growth rate analysis of WT and various FSH deletion mutant yeast strains under H2O2 conditions.
- Phenotypic analysis of FSH3 overexpression in WT and mutant yeast strains, assessing apoptosis markers and cell viability.
Main Results:
- H2O2 exposure significantly increased both mRNA and protein levels of FSH3 in WT yeast.
- Deletion of FSH3 enhanced yeast growth under H2O2-induced stress, while FSH3 overexpression led to apoptosis.
- FSH3 overexpression inhibited growth in all double deletion mutants, but not in cells lacking NUC1, indicating NUC1-dependent apoptosis induction.
Conclusions:
- FSH3 plays a crucial role in the yeast response to oxidative stress, mediating apoptosis.
- The pro-apoptotic function of FSH3 is dependent on the presence of NUC1.
- FSH3 represents a potential target for understanding and manipulating cellular responses to oxidative damage.
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