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Mitochondrial Respiration Quantification in Yeast Whole Cells
Published on: November 8, 2024
Redox responses in yeast to acetate as the carbon source
Karyl I Minard1, L McAlister-Henn
1Department of Biochemistry, University of Texas Health Science Center, San Antonio, 78229-3900, USA.
Archives of Biochemistry and Biophysics
|January 14, 2009
Summary
Yeast cells shift their NAD(P)H cofactor levels when utilizing acetate. Both salvage and de novo pathways are crucial for NAD(P)H biosynthesis and cellular viability, especially in mutant strains.
Area of Science:
- Biochemistry
- Yeast Metabolism
- Cellular Respiration
Background:
- Cellular metabolism relies on redox cofactors like NAD(P)+/NAD(P)H.
- Acetate utilization in yeast involves complex metabolic shifts.
- Isocitrate dehydrogenase (IDH) is a key enzyme in the tricarboxylic acid cycle.
Purpose of the Study:
- Investigate the impact of acetate as a carbon source on yeast cofactor levels.
- Determine the role of NAD(P)H biosynthesis pathways in yeast viability.
- Characterize the metabolic behavior of an IDH-deficient yeast mutant.
Main Methods:
- Shifting yeast strains (parental and idhDelta mutant) to acetate medium.
- Measuring total cellular NAD(P)+NADH and the NAD(P)+/NAD(P)H ratio.
- Assessing the importance of salvage and de novo NAD(P)H biosynthesis pathways.
Main Results:
- Parental yeast showed a transient decrease in total NAD(P)H but a 10-fold increase in the NAD(P)+/NAD(P)H ratio.
- The idhDelta mutant had higher total NAD(P)H but similar ratio changes, despite impaired growth.
- Salvage pathway was vital for parental strain viability; idhDelta mutant relied on both salvage and de novo pathways.
Conclusions:
- NAD(P)H homeostasis is critical for yeast adaptation to acetate.
- Both salvage and de novo pathways are essential for yeast viability, particularly in IDH-deficient mutants.
- Oxygen consumption is unaffected, suggesting NAD(P)H supports other cellular functions.
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