Plant-parasitic nematodes cause billions of dollars' worth of agricultural damage annually. Although resistant cultivars and nematicides have been used to control nematodes, there exists a need for more effective treatment strategies. Plants are known to respond to plant-parasitic nematodes similar to other pathogens; however, the underlying molecular mechanism remains elusive. Nematodes use molecules from a conserved pheromone family, the ascarosides, to regulate developmental and social behaviors. Previously, we have shown that ascr#18, the major ascaroside in the plant-parasitic nematodes, elicits plant defense response in monocots and dicots, improving their resistance to nematodes, bacterial and fungal pathogens. In recent work, we demonstrated that ascr#18 is taken up by Arabidopsis and tomato, metabolized into shorter side-chained ascarosides, and secreted into the rhizosphere via the roots. The identity of ascr#18 and metabolized ascarosides was confirmed by LC-MS/MS and using 13C-labeled derivatives. Since nematodes use peroxisomal ?-oxidation pathway to metabolize ascarosides, we investigated ascaroside metabolism in several Arabidopsis mutants defective in this pathway. Interestingly, a mutant defective in production of two acyl-CoA oxidases,
acx1/acx5, is unable to metabolize ascr#18. In addition, we have shown that
acx1/acx5 mutant is compromised in ascr#18-mediated enhanced resistance to root-knot nematodes. Our results suggest that plants use conserved metabolic pathways to process ascr#18 into its derivatives, thereby modifying the composition of their root exudates to regulate their interaction with nematodes