Action mechanism of a novel herbicide, fenoxasulfone

The action mechanism of fenoxasulfone was studied by examining the inhibitory effects of this herbicide on the biosynthesis of very-long-chain fatty acids (VLCFAs). Fenoxasulfone treatment decreased VLCFAs, such as C20:0, C20:1, C22:0, C24:0, C24:1 and C26:0 fatty acids, in barnyard millet cultured cells, and increased long-chain-fatty acids and medium-chain-fatty acids, such as C18:0 and C15:0, which are precursors of VLCFAs. Fenoxasulfone potently inhibited activities of VLCFA elongase (VLCFAE) in the microsomal fraction of etiolated barnyard millet seedlings, which catalyzed the elongation steps from C22:0 to C24:0 and C24:0 to C26:0, respectively. These results strongly suggested that fenoxasulfone is a potent inhibitor of plant VLCFAEs and should be categorized within the K3 group of the Herbicide Resistance Action Committee. VLCFAE activity of recombinant Fatty Acid Elongation 1 (FAE1) of Arabidopsis that catalyzes the elongation step from C18:1 to C20:1, was inhibited by fenoxasulfone in a time-dependent manner, which has been shown in the inhibition of VLCFAEs by other well-known VLCFAE-inhibiting herbicides. On the other hand, VLCFAE activity of the microsomal fraction of etiolated barnyard millet seedlings, which catalyzes the elongation step from C24:0 to C26:0, was inhibited by fenoxasulfone in a time-independent manner. This time-independent inhibition raised a new inhibition mechanism of VLCFAE by fenoxasulfone likely with pyroxasulfone, which is classified in the same chemical class as fenoxasulfone.