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Electron-Transferring Flavoprotein and Its Dehydrogenase Required for Fungal Pathogenicity in Arthrobotrys oligospora
Yonglan Liu1, Zhangyu Li1, Junjie Liu1
1State Key Laboratory for Conservation and Utilization of Bio-Resources in Yunnan, Yunnan University, Kunming 650091, China.
Abstract:
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. Arthrobotrys oligospora is a typical invasion fungus to nematodes. Its ETF characterization is still unknown. Here, we showed that the mutations of A. oligospora ETF (Aoetfα and Aoetfβ) and its dehydrogenase (Aoetfdh) 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 Aoetfβ beyond all induction cues. Moreover, the deletion of Aoetfβ has led to the accumulation of butyrate-like smell, which has a strong attraction to Caenorhabditis elegans 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.
Insights
Electron transfer flavoprotein (ETF) is crucial for nematode-trapping fungi like Arthrobotrys oligospora, impacting metabolism and predatory behavior. Mutations disrupt mitochondrial function and trap formation, affecting nematode interactions.
Area of Science:
- Biochemistry
- Mycology
- Molecular Biology
Background:
- Electron transfer flavoprotein (ETF) is vital in fatty acid oxidation and amino acid metabolism.
- Fungal ETF can influence opportunistic fungal pathogenicity by altering cellular metabolites.
- Arthrobotrys oligospora is a nematode-invading fungus with uncharacterized ETF function.
Purpose of the Study:
- To characterize the role of ETF and its dehydrogenase in Arthrobotrys oligospora.
- To investigate the impact of ETF mutations on fungal metabolism and pathogenicity.
- To understand the regulation of nematode-trapping and fungal-nematode interactions.
Main Methods:
- Gene knockout/mutation of Aoetfα, Aoetfβ, and Aoetfdh in Arthrobotrys oligospora.
- Analysis of mitochondrial integrity and fatty acid metabolism.
- Assessment of trap formation in response to nematode signals and nutrients.
- Evaluation of nematode predatory activity and attraction.
Main Results:
- Mutations in Aoetfα, Aoetfβ, and Aoetfdh caused severe mitochondrial defects and blocked fatty acid metabolism.
- Pathogenicity-related trap structures were suppressed by nematode signals and nutrients (ammonia, urea).
- Nematode predatory activity was reduced and delayed in mutants; however, rich nutrition restored trap formation and activity in Aoetfβ mutants.
- Aoetfβ deletion resulted in butyrate-like odor attracting Caenorhabditis elegans.
Conclusions:
- ETF and its dehydrogenase are essential for nematode-trapping fungi, regulating mitochondrial metabolism.
- Mitochondrial metabolite fluctuations are linked to fungal pathogenesis and nematode interactions.
- ETF function influences the complex relationship between fungi and their nematode hosts.
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