The formation of the trapping device induced by nematodes has been assumed as an indicator for a switch from saprophytic to predacious lifestyles for nematode-trapping fungi. However, fungal nematocidal activity is not completely synonymous with fungal trap formation. We found that the predominant nematode-trapping fungus harbored a rare () gene cluster that was mainly distributed in nematode-trapping fungi.
View Article and Find Full Text PDFOur previous study reported that seminaturally occurring arthrocolins A to C with unprecedented carbon skeletons could restore the antifungal activity of fluconazole against fluconazole-resistant Candida albicans. Here, we showed that arthrocolins synergized with fluconazole, reducing the fluconazole minimum and dramatically augmenting the survivals of 293T human cells and nematode Caenorhabditis elegans infected with fluconazole-resistant C. albicans.
View Article and Find Full Text PDFThe predominant nematode-trapping fungus harbors a unique polyketide synthase-prenyltransferase (PKS-PTS) gene cluster responsible for the biosynthesis of sesquiterpenyl epoxy-cyclohexenoids (SECs) that are involved in the regulation of fungal growth, adhesive trap formation, antibacterial activity, and soil colonization. However, the function of one rare gene ( ()) embedded in the cluster has remained cryptic. Here, we constructed two mutants with the disruption of and the overexpression of , respectively, and compared their fungal growth, morphology, resistance to chemical stress, nematicidal activity, transcriptomic and metabolic profiles, and infrastructures, together with binding affinity analysis.
View Article and Find Full Text PDFSesquiterpenyl epoxy-cyclohexenoids (SECs) that depend on a polyketide synthase-terpenoid synthase (PKS-TPS) pathway are widely distributed in plant pathogenic fungi. However, the biosynthesis and function of the acetylated SECs still remained cryptic. Here, we identified that 00215 273 (273) was responsible for the acetylation of SECs in via the construction of Δ273, in which the acetylated SECs were absent and major antibacterial nonacetylated SECs accumulated.
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