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Mitochondrial heterogeneity drives the evolution of fungicide resistance in Phytophthora sojae, with associated fitness trade-offs

Summary

Researchers studied how a plant pathogen called Phytophthora sojae develops resistance to the fungicide ametoctradin. They found that resistance builds up gradually through changes in mitochondrial DNA, where a single mutation accumulates over generations. While this mutation helps the fungus survive the fungicide, it damages its mitochondria and reduces its overall fitness, though the organism can partially compensate through increased expression of a protein called TFAM1.

Background

Ametoctradin, a mitochondrial complex III inhibitor, is crucial for controlling oomycete diseases. However, increasing fungicide resistance threatens disease management effectiveness. Understanding resistance evolution mechanisms is essential for optimizing disease control strategies.

Objective

To elucidate the evolutionary mechanisms of ametoctradin resistance in Phytophthora sojae and identify the roles of mitochondrial heteroplasmy and fitness trade-offs in driving resistance evolution.

Results

The PsCytb S33L mutation directly confers ametoctradin resistance through mitochondrial heteroplasmy accumulation. Low-, medium-, and high-resistant mutants serve as transitional populations, with resistance levels correlating to PsCytb L33 mutation abundance. Resistant strains exhibit mitochondrial dysfunction with elevated ROS levels, reduced membrane potential, and increased mtDNA copy number, accompanied by upregulation of TFAM1.

Conclusion

Mitochondrial heterogeneity drives ametoctradin resistance evolution in P. sojae through PsCytb S33L mutation accumulation. Resistance evolution involves both standing variation and de novo mutations. The PsCytb S33L mutation causes significant fitness trade-offs, partially offset by TFAM1 upregulation, revealing coevolution of mitochondrial and nuclear genomes.
  • Published in:Science Advances,
  • Study Type:Experimental Laboratory Study,
  • Source: PMID: 41576162, DOI: 10.1126/sciadv.adz4601
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