Herbicides are defined as a chemical substance that is used to eliminate unwanted plants. This is a very general description and it is important to remember that herbicides differ with respect to when they are used (for example, pre-emergence or post-emergence), their activity (for example, contact or systemic), their selectivity (for example, grasses or broadleaves), and their mechanism of action (also known as: mode of action, site of action). (See this blog post about basic herbicide terminology:http://ucanr.org/blogs/blogcore/postdetail.cfm?postnum=5973)
What is a mechanism of action? The mechanism of action (MOA) is the way the herbicide controls susceptible plants. More specifically, it describes the biological processes that are disrupted by the herbicide. These biochemical pathways control the growth and development of plants; when herbicides are applied, these processes cannot be carried out and plant injury and death will occur.
Where can I find out information about the MOA's? The Weed Science Society of America (WSSA) lists all herbicide MOAs in a downloadable fact sheet. http://www.wssa.net/Weeds/Resistance/WSSA-Mechanism-of-Action.pdf
What do MOAs have to do with herbicide resistance? The over-reliance (across acres and time) on one MOA for weed control in an agricultural system can increase the probability of selecting for an herbicide-resistant population. With repeated applications, susceptible individuals of a target weed species will die off while the numbers of resistant plants will continue to grow. With time, the MOA will no longer control that species in that location. The chances of the population reverting back to a susceptible state are low. To prevent/mitigate herbicide resistance, it is advised to rotate herbicide MOAs to reduce the selective pressure applied by any one product. Note: Several MOAs are comprised of multiple chemical families that are alike with respect to chemical structure and cause similar injury symptoms. Rotating between chemical families within an MOA is not the same as rotating among MOAs.
So, what MOAs do we have available in orchards and vineyards in California?
WSSA Group 1: Inhibition of acetyl CoA carboxylase (ACCase)
What does that mean? These herbicides inhibit the creation of lipids in grasses (broadleaved weeds are usually not affected). Lipids are the principal components of plant cell membranes; if lipid biosynthesis is inhibited, the plant will be unable to produce new plant cells, which are necessary for continued plant growth.
Examples: clethodim (Prism), fluazifop (Fusilade), sethoxydim (Poast)
WSSA Group 2: Inhibition of acetolactate synthase (ALS)
What does that mean? ALS inhibitors stops the production of three amino acids (isoleucine, leucine, and valine), which, in turn stops the production of enzymes and other proteins that are built from these amino acids.
Examples: halosulfuron (Sandea), rimsulfuron (Matrix), penoxsulam (PindarGT)
WSSA Group 3: Inhibition of mitosis
What does that mean? These herbicides inhibit cell division in germinating seedlings and stop lateral root formation. Lateral roots are important for the uptake of water and nutrients from the soil.
Examples: pendimethalin (Prowl H2O), oryzalin (Surflan)
WSSA Group 4: Growth regulators
What does that mean? These herbicides mimic auxin, a naturally produced growth regulator. Although their activity is not completely understood, auxins are known to have roles in cell elongation and cell wall formation, and are known to control lateral growth. Symptoms of their use are distinctive; broadleaved weeds treated with these growth regulators have stems that are often twisted and curled, malformed flowers, thickened or stunted roots, and have cupped, strapped or otherwise deformed leaves.
Examples: 2,4-D
WSSA Groups 5 and 7: Inhibition of photosystem II (PSII)
What does that mean? These herbicides prevent normal transfer of the energy collected from sunlight in the photosynthetic pathway where it is normally used to generate sugars needed for plant growth. Because energy is still being taken in, but is not properly passed along, the now excess energy generates highly reactive free radicals that cause damage to chlorophyll and cell membranes.
Examples: simazine (Princep), diuron (Karmex)
WSSA Group 8: Fatty acid and lipid biosynthesis inhibitors
What does that mean? These herbicides inhibit several plant processes including the synthesis of fatty acids and lipids that may account for reductions in cuticular waxes and the synthesis of proteins, gibberellins and anthocyanins.
Examples: EPTC (EPTAM)
WSSA Group 9: Inhibition of enolpyruvyl shikimate-3-phosphate synthase (EPSPS)
What does that mean? Glyphosate inhibits EPSPS, which stops the production of three aromatic amino acids (tryptophan, phenylalanine, and tyrosine) that are produced through the shikimate pathway. This, in turn, stops the production of enzymes and other proteins that are subsequently built from these amino acids. The shikimate pathway is very important for plant growth; by some estimates, 20% of all carbon fixed in the leaves passes through the shikimate pathway.
Examples: glyphosate (Roundup)
WSSA Group 10: Inhibition of glutamine synthetase
What does that mean? Glutamine synthetase inhibitors stop the conversion of two chemicals, glutamate and ammonia, to glutamine, which allows for an accumulation of ammonia in the plant. Ammonia inhibits photosynthesis and can destroy plant cells.
Examples: glufosinate (Rely 280)
WSSA Group 12: Carotenoid biosynthesis inhibitors
What does that mean? Carotenoids harvest light and transfer the captured energy to chlorophyll molecules. They also have antioxidant properties that help protect chlorophyll from reactive molecules. The absence of carotenoids allows for the destruction of chlorophyll, which is needed for photosynthesis.
Examples: norflurazon (Solicam)
WSSA Group 14: Inhibition of protopophyrinogen oxidase (PPO)
What does that mean? Protoporphyrinogen oxidase (PPO) is an enzyme that catalyzes a biological reaction that is involved in the production of chlorophyll. PPO inhibitors block the production of chlorophyll. More importantly, they cause reactive molecules to form in the cell, which, in turn, destroy existing chlorophyll molecules, carotenoids and destroy cell membranes.
Examples: flumioxazin (Chateau), saflufenacil (Treevix), carfentrazone (Shark), pyraflufen (Venue)
WSSA Group 15: Inhibition of mitosis
What does that mean? These herbicides inhibit the production of very long chain fatty acids and prevent seedlings from developing properly.
Examples: napropamide (Devrinol)
WSSA Groups 20, 21, 29: Cellulose inhibitors
What does that mean? These herbicides inhibit cell wall synthesis; cell walls are necessary for plant growth.
Examples: dichlobenil (Casoron), isoxaben (Trellis), indaziflam (Alion)
WSSA Groups 22: Inhibition of photosystem I (PSI)
What does that mean? These herbicides accept electrons from the photosynthetic pathway that leads to the formation of reactive molecules that destroy lipids, which in turn leads to the breakdown of plant cell membranes.
Examples: paraquat (Gramoxone Inteon), diquat (Diquat)
In general, where can I find out information about a specific herbicide's MOA? This information is sometimes, but not always, found on the herbicide label. Some manufacturers will directly specify which WSSA group the herbicide belongs to (hypothetical example: Group 9, Glycines), while others will verbally describe the herbicide's MOA in the product description section of the label (hypothetical example: this product inhibits the enzyme, EPSP synthase). If you are unsure …ASK!
So, if I just rotate my MOAs I'll be okay, right? If only it were that easy. Rotating chemicals is a start, but there is more to be done than just that. When/if possible: rotate/alternate crops, use certified seed, cultivate, hand-weed, mulch or inter-crop, prevent weeds from going to seed in fields and orchards, prevent weed seed from being dispersed on farm equipment, etc… And remember to scout. Evaluate weed populations BEFORE and AFTER weed control strategies are employed; this will allow you to detect potentially resistant populations early and manage them most effectively.
NOTE: NOT ALL MOAs ARE AVAILABLE IN ALL CROPS! READ LABELS AND CONSULT PCAs AND FARM ADVISORS BEFORE APPLYING!
This blog is an extension of a previous post: http://ucanr.org/blogs/blogcore/postdetail.cfm?postnum=6404
