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Yeast Model System Showed That Heterologously Expressed Mutant Atp9 Has a Negative Impact on Cell Growth by Causing
Takeshi Ito1, Kenta Terai2,3, Hidetaka Kosako2
1Graduate School of Agriculture, Ehime University, 3-5-7 Tarumi, Matsuyama, Ehime 790-8566, Japan.
Biological & Pharmaceutical Bulletin
|July 24, 2025
Summary
Targeting ATP depletion via mutant mitochondrial ATP synthase subunits offers a novel strategy against pests, pathogens, and cancer. Introducing a single mutated Atp9 subunit inactivates the enzyme, depleting cellular ATP.
Area of Science:
- Biochemistry
- Molecular Biology
- Cellular Respiration
Background:
- ATP depletion is a viable strategy for controlling pests, pathogens, and cancer cells.
- Mitochondrial F1Fo-ATP synthase is a key target due to its role in oxidative phosphorylation.
Purpose of the Study:
- To investigate the potential of heterologous expression of mutant Atp9 subunits to deplete intracellular ATP.
- To validate this approach as a method for controlling target cells and organisms.
Main Methods:
- Utilized a yeast model system for experimental validation.
- Conducted a series of biochemical analyses to assess ATP synthase function and cellular ATP levels.
Main Results:
- Confirmed that a single mutated Atp9 subunit (glutamic acid to glutamine substitution) is sufficient to abrogate ATP synthase function.
- Demonstrated that heterologous expression of mutant Atp9 leads to the assembly of nonfunctional ATP synthase complexes.
- Verified significant depletion of intracellular ATP in the yeast model.
Conclusions:
- The hypothesis that heterologous expression of mutant Atp9 can lead to ATP depletion was validated.
- This strategy offers a promising method for developing new agents against pests, pathogens, and cancer.
- Targeting mitochondrial ATP synthase function presents a novel therapeutic avenue.
