Plant & Soil Sciences eLibraryPRO
control panel control panel

Inhibitors of Fatty Acid Synthesis and Elongation

Rate Me


Herbicides inhibit several different elongases, each with different enzymatic functions.  Long-chain fatty acid:CoA ligase (EC is inhibited by the carbamothioate herbicides EPTC and triallate.  However, details about other elongases inhibited by these herbicides are unknown.
      Carbamothioates:  These soil-applied herbicides inhibit early seedling development, primarily the emergence and elongation of primary shoots.  One of the first documented injury symptoms of EPTC was a reduction 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 enzymes in plants.
      Carbamothioate herbicides are actually pro-herbicides, 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 endogenous sulfoxidase enzymes in order to become phytotoxic
      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 herbicide safeners, 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 glutathione production, and enhanced glutathione transferase and cytochrome P450 enzyme activity.  The result is that crop plants are better able to metabolize and detoxify 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 degradation has been termed ‘enhanced degradation’ and ‘preconditioned soil’.

  Carbamothioate Family
 Base Structure and Examples
Butylate = Sutan+
Triallate = Far-Go
Cycloate = Ro-neet    
Thiobencarb = Bolero, Saturn
EPTC = Eptam or Eradicane (when mixed with a safener)
Vernolate = Vernam
Molinate = Ordram
Metham = Vapam
Pebulate = Tillam
 Field Use Used for preemergence control of annual grasses, purple and yellow nutsedge, and annual broadleaf weeds (some members).  Usually incorporated mechanically or with irrigation immediately after application to avoid vapor losses.  Sometimes applied as granules to the soil surface or metered into irrigation (chemigation).
 Selectivity Selectivity obtained by herbicide placement, usually in a treated zone above crop seeds; safener treatment of crop seed induces herbicide conjugation and inactivation
 Symptoms First seedling leaf is distortion and usually fails to emerge from coleoptile; emerged seedlings remain small and die quickly
 Absorption and Translocation Quickly absorbed by roots and slowly translocated to shoots
 Plant Metabolism Tolerant plants rapidly metabolize the herbicides; susceptible plants activate parent compound (some members) so that it becomes herbicidal
 Soil Activity Usually persist for 3 to 6 weeks; continuous use selects for soil microbes that rapidly degrade the herbicides (‘preconditioned soil’)

Chloroacetamides:  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. 

  Chloroacetamide Family
 Sample  Structure and Examples   Propachlor =    Ramrod
Acetochlor = Surpass, Harness Plus
Alachlor = Lasso    
Metolachlor = Dual (II) Magnum
Dimethenamid = Outlook    
Butachlor = Machete
 Field Use Applied PPI or PRE as liquid sprays or granular applications for selective preemergence control of annual grasses and some broadleaf weeds 
 Selectivity Biochemical basis for selectivity not known in detail; ‘natural’ tolerance in plants based on metabolism; safener treatment of crop seed can confer tolerance
 Symptoms Seeds of sensitive plants usually germinate, but the seedlings either do not emerge or show abnormal growth
 Absorption andTranslocation Readily absorbed by roots and/or shoots of germinating seedlings and slowly translocated in the apoplast
 Metabolism in the plant Tolerant plants rapidly metabolize the herbicides; conjugation to glutathione is common
 Soil activity Usually persist for 5 to 8 weeks; leaching can be a problem after heavy precipitation

Resistance to Very Long Chain Fatty Acid (VLCFA) Inhibitors 

    Resistance to the carbamothioate herbicide triallate did not evolve until it had been used for more than 25 years.  Wild oat (Avena fatua) populations resistant to triallate were first documented in 1990 in Alberta and subsequently reported in Montana.  The resistant biotypes are unusual, because they represent metabolic loss-of-function mutants.  Carbamothioate herbicides are actually pro-herbicides, in that they require metabolic activation by sulfoxidase enzymes to become phytotoxic.  In Montana, the resistant biotype was 10- to 15-fold slower at converting the triallate pro-herbicide into the phytotoxic triallate sulfoxide.  Both biotypes were equally susceptible to synthetic triallate sulfoxide, and the metabolism rates of this toxic form were equivalent.  Resistance was conferred by two recessive nuclear genes, 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 selection pressure.  First, even though triallate has a reasonably long soil half-life, its precise application requirements rarely allow it to achieve greater than about 85% wild oat control, and so it exerts less selection pressure compared to some other herbicides.  Second, the target species (wild oat) has relatively low seed production and poor seed dispersal, traits that tend to limit population sizes and thus reduce the frequency of potentially resistant individuals.  And third, the necessity of accumulating two separate recessive alleles 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 time.  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 germination was higher in the resistant lines
    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.


Be the first to write a comment...

Control Panel cancel

Create activities for your moodle courses. Moodle Go to moodle
Select and group e-Library Lessons to create your own package... My Communities
Community Blogs Community Media

My Joined Communities

My Blogs - a journal of my thoughts... My Blogs
My Comments - my thoughts expressed as a feedback... My Comments
Classes that I am taking Registered Classes
Class Blogs Class Media
Check the scores of assesments that you have taken Taken Assessments
Please confirm your selection.