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Updated: Jun 16, 2026

Mitochondrial Respiration Quantification in Yeast Whole Cells
Published on: November 8, 2024
The Pseudomonas fluorescens secondary metabolite 2,4 diacetylphloroglucinol impairs mitochondrial function in
Olive Gleeson1, Fergal O'Gara, John P Morrissey
1Department of Microbiology, University College Cork, Cork, Ireland.
Abstract:
Pseudomonas fluorescens strains are known to produce a wide range of secondary metabolites including phenazines, siderophores, pyoluteorin, and 2,4 diacetylphloroglucinol (DAPG). DAPG is of particular interest because of its antifungal properties and because its production is associated with inhibition of phytopathogenic fungi in natural disease-suppressive soils. This trait has been exploited to develop strains of P. fluorescens that have potential application as biocontrol agents. Although the biochemistry, genetics and regulation of DAPG production have been well-studied, relatively little is known about how DAPG inhibits fungal growth and how fungi respond to DAPG. Employing a yeast model and a combination of phenotypic assays, molecular genetics and molecular physiological probes, we established that inhibition of fungal growth is caused by impairment of mitochondrial function. The effect of DAPG on yeast is largely fungistatic but DAPG also induces the formation of petite cells. Expression of the multidrug export proteins Pdr5p and Snq2p is increased by DAPG-treatment but this appears to be a secondary effect of mitochondrial damage as no role in enhancing DAPG-tolerance was identified for either Pdr5p or Snq2p.
Insights
Pseudomonas fluorescens produces 2,4-diacetylphloroglucinol (DAPG), an antifungal compound. This study reveals DAPG inhibits fungal growth by impairing mitochondrial function, leading to fungistasis and petite cell formation in yeast.
Area of Science:
- Microbiology
- Biochemistry
- Mycology
Background:
- Pseudomonas fluorescens produces antifungal compounds like 2,4-diacetylphloroglucinol (DAPG).
- DAPG is linked to disease suppression in soils and has potential as a biocontrol agent.
- Mechanisms of DAPG's antifungal action and fungal responses are poorly understood.
Purpose of the Study:
- To investigate how DAPG inhibits fungal growth.
- To understand fungal responses to DAPG exposure.
- To elucidate the role of specific yeast proteins in DAPG tolerance.
Main Methods:
- Utilized a yeast model system.
- Conducted phenotypic assays and molecular genetics.
- Employed molecular physiological probes to assess mitochondrial function.
Main Results:
- DAPG inhibits fungal growth by impairing mitochondrial function.
- DAPG exhibits fungistatic effects and induces petite cell formation in yeast.
- Increased expression of Pdr5p and Snq2p is a secondary effect of mitochondrial damage, not conferring DAPG tolerance.
Conclusions:
- DAPG's antifungal activity stems from mitochondrial dysfunction.
- Yeast response to DAPG involves fungistasis and petite cell induction.
- Multidrug efflux pumps are not primary mediators of DAPG tolerance.
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