Electron-Transferring Flavoprotein and Its Dehydrogenase Required for Fungal Pathogenicity in Arthrobotrys oligospora

Electron transfer flavoprotein (ETF) plays an important function in fatty acid beta oxidation and the amino acid metabolic pathway. It can provide pathogenicity to some opportunistic fungi via modulating cellular metabolite composition. <i>Arthrobotrys oligospora</i> is a typical invasion fungus to nematodes. Its ETF characterization is still unknown. Here, we showed that the mutations of <i>A. oligospora</i> ETF (<i>Aoetfα</i> and <i>Aoetfβ</i>) and its dehydrogenase (<i>Aoetfdh</i>) led to severe defects in mitochondrial integrity and blocked fatty acid metabolism. The pathogenicity-associated trap structures were completely suppressed when exposed to nematode-derived ascarosides and nutrition signals, including ammonia and urea. Compared to the wild-type strain, the nematode predatory activity was significantly reduced and delayed. But surprisingly, the rich nutrition could restore the massive trap and robust predatory activity in the mutant <i>Aoetfβ</i> beyond all induction cues. Moreover, the deletion of <i>Aoetfβ</i> has led to the accumulation of butyrate-like smell, which has a strong attraction to <i>Caenorhabditis elegans</i> nematodes. Ultimately, ETF and its dehydrogenase play a crucial role in nematode-trapping fungi, highlighting mitochondrial metabolite fluctuations that are connected to pathogenesis and further regulating the interactions between fungi and nematodes.