Regulation of Cholesterol and Fatty Acid Synthesis
Herbicides inhibit several different elongases, each with different enzymatic functions. Long-chain fatty acid:CoA (EC 184.108.40.206) is inhibited by the carbamothioate herbicides EPTC and triallate. However, details about other elongases inhibited by these herbicides are unknown.
: These soil-applied herbicides inhibit early development, primarily the emergence and elongation of primary . One of the first documented injury symptoms of EPTC was a in cuticular wax deposition. Other severe injury symptoms include the failure of leaf emergence from the coleoptile and a general stunting of seedling growth, indicating that inhibition of VLCFA synthesis has many, widespread effects on normal plant growth. This observation also supports the idea that there may be other functions for elongation in plants.
Carbamothioate herbicides are actually , in that the form of the herbicide applied to plants (the parent molecule) is not toxic. Once the parent molecule is absorbed into plant tissues, it must be cleaved and metabolically activated by in order to become .
Carbamothioates are soil applied and can be applied as pre-plant incorporated or pre-emergence herbicides. Crop selectivity depends upon planting crop seeds below the treated soil. Such manipulations are sometimes hard to achieve with precision, and so crop injury from these herbicides is a recurring problem. The potential for crop injury led to early research on compounds known as , antidotes, or protectants. The first safeners thus identified were used to protect corn from EPTC injury, and include the compounds naphthalic anhydride, benoxacor, fenclorim, and fluxofenim. Safeners are coated onto crop seeds or may be mixed with some commercial herbicide formulations. They commonly induce one or more plant defense mechanisms, including increased production, and enhanced and activity. The result is that crop plants are better able to metabolize and the herbicide. Interestingly, these compounds protect monocot but not dicot crops from herbicide injury, for reasons that are not entirely clear.
Carbamothioate herbicides have been shown to cause changes in the makeup of soil microbial communities. In particular, continuous usage in the same field selects for bacteria and actinomycetes that rapidly degrade these herbicides, to the extent that they are essentially ineffective for weed control. This phenomenon of rapid herbicide has been termed ‘enhanced degradation’ and ‘preconditioned soil’.
: The chloroacetamide family is one of the most widely used groups of herbicides in the world, primarily due to the use of metolachlor. The first member of this family to be commercialized was alachlor by the Monsanto Company in 1969. They are extensively used in corn and soybeans to control a broad spectrum of annual grasses and some broadleaf weeds. They are soil applied and usually do not require soil incorporation for activity. Herbicides in this family inhibit plastidic VLCFA synthesis, although the precise enzymatic step(s) are not known.
to the carbamothioate herbicide triallate did not evolve until it had been used for more than 25 years. Wild oat (Avena fatua) populations to triallate were first documented in 1990 in Alberta and subsequently reported in Montana. The resistant biotypes are unusual, because they represent metabolic . Carbamothioate herbicides are actually pro-herbicides, in that they require metabolic activation by sulfoxidase enzymes to become phytotoxic. In Montana, the resistant was 10- to 15-fold slower at converting the triallate into the phytotoxic triallate sulfoxide. Both biotypes were equally susceptible to synthetic triallate sulfoxide, and the rates of this toxic form were equivalent. Resistance was conferred by two nuclear , which may encode the enzymes responsible for triallate sulfoxidation. The mechanism of resistance in the Canadian biotype appears to involve alterations in gibberellin biosynthesis. Interestingly, both biotypes are cross-resistant to difenzoquat, an unrelated pyrazolium herbicide.
Triallate was used for about 30 years before resistant biotypes appeared in agricultural fields. This unusually long, resistance-free usage period illustrates several important concepts about plant responses to herbicide . First, even though triallate has a reasonably long soil , its precise application requirements rarely allow it to achieve greater than about 85% wild oat control, and so it exerts less pressure compared to some other herbicides. Second, the target (wild oat) has relatively low seed production and poor seed dispersal, traits that tend to limit population sizes and thus reduce the of potentially resistant individuals. And third, the necessity of accumulating two separate recessive to achieve resistance in self-pollinating wild oats would require a large number of individuals and generations. If carbamothioate herbicides in fact inhibit several elongases, the accumulation of additional alleles would require even more . It might be expected that the loss of two sulfoxidase-like activities would be associated with a fitness cost in the resistant biotype. While fitness comparisons have not been done for the Montana biotypes, studies of the Canadian biotypes did not support this idea, and in fact seed was higher in the resistant .
Resistance to chloroacetamide herbicides has only been verified for barnyardgrass (China) and rigid ryegrass (Australia), and in both cases is based on enhanced metabolism. The scarcity of resistant species is surprising, considering the long history and widespread use patterns of these herbicides.