Verification of Resistance Mechanism of Mitochondrial Electron Transport Chain Complex III Inhibitors in <i>Phytophthora sojae</i> through Ectopic Overexpression

While Cytb point mutations are recognized as a contributing factor to the resistance of plant pathogens against mitochondrial electron transport chain (mETC) complex III inhibitors, there remains a notable absence of direct genetic transformation data. In this study, we verified that 24 point mutations increase the resistance of <i>Phytophthora sojae</i> to different types of mETC complex III inhibitors through ectopic expression of the <i>PsCytb</i> gene. Notably, S33L, F220L, and M124I mutations confer resistance to certain inhibitors, while simultaneously increasing sensitivity to other types of mETC complex III inhibitors. Molecular docking results demonstrated that variations in binding energy between PsCytb harboring different point mutations and various mETC complex III inhibitors constitute the primary mechanism underlying these negative cross-resistances. Our research findings offer strategic guidance for managing fungicide resistance and designing novel fungicides targeting mETC complex III.