How do selective herbicides work?
Most chemical users at some time or another, have wondered how selective herbicides actually work, and how they 'select' the weeds and leave the useful plants alone.
The common phenoxy herbicides, such as 2,4-D and MCPA, are selective for broadleaf weeds and work by disrupting the fine balance of biochemical processes that occur in these weeds.
The phenoxy herbicides mimic a naturally occurring plant chemical called Indole Acetic Acid (IAA). They cause unregulated IAA production in the plant, which leads to uncontrolled growth, twisting, thickening, elongation, and eventually death as the weed literally grows itself to death.
Other selective herbicides target photosynthesis, the process where plants produce energy from sunlight. Normally, blocking photosynthesis would result in a very slow death for weeds as they starve to death however these herbicides seem to work too quickly for this to be the case.
Scientists think that blocking photosynthesis is only part of the story. The other thing that may happen when photosynthesis is blocked is that highly toxic oxygen and hydroxyl compounds form within the weed. These compounds rapidly destroy cell membranes, causing the weed to die.
Many selective herbicides target enzymes within plant cells. Enzymes are proteins that work as catalysts in many processes within cells, allowing complex chemical reactions to occur under conditions where they probably otherwise wouldn't occur.
Enzyme activity in plants normally occurs in a controlled state of equilibrium. When a herbicide targets an enzyme site, it disrupts the sequence of complex chemical reactions, and in many cases, produces highly toxic compounds in the plant, which kills the weed.
A number of the grass selective herbicide products are not herbicidal when stored in their original container. This is because they are manufactured as 'proherbicides' that change into the active chemical form once inside the weed.
An example of proherbicides are grass selective herbicides containing diclofop-methyl. Diclofop-methyl is a proherbicide, not a herbicide. Once it is applied and absorbed by the leaves of the weed, an enzyme in the plant cells removes the methyl group from the diclofop, and the diclofop then kills the weed by inhibiting the production of an enzyme that assists fatty acid synthesis.
Fatty acids are an integral part of cell membranes, waxes and the leaf cuticle. When fatty acid production stops, the weed dies because it cannot continue to carry on the basic biological processes essential for life.
So why don't selective herbicides kill the useful plants we are trying to grow? The main reason is because the useful plants are able to metabolise (break down) the herbicide more rapidly than the weeds, allowing them to survive. In other cases such as 2,4-DB, some useful plants are unable to break it down into the active form of 2,4-D, thus they survive while weeds that can break down to 2,4-D do not.
The development of herbicide resistant weeds has been a real issue impacting sustainable weed control for over 20 years.
Herbicide resistance occurs when a plant that would normally be controlled by a herbicide, survives the application of a usually lethal rate, and the change that caused the resistance is heritable. If the change is heritable, it can be passed on to succeeding generations of the weed by seeds.
For a number of years, herbicides have been grouped by their mode of action to allow herbicide resistance to be managed. The table below shows the current Mode of Action groups for herbicides in Australia (as of June 2013 – source: CropLife Australia website).
|Resistance Risk||Mode of Action Group||Typical Actives|
|High||A||clethodim, diclofop, fluazifop, haloxyfop, propaquizafop, sethoxydim|
|B||chlorsulfuron, flumetsulam, halosulfuron, imazapyr, metsulfuron, triasulfuron|
|Moderate||C||atrazine, bromoxynil, diuron, linuron|
|D||chlorthal, oryzalin, pendimethalin|
|F||diflufenican, norflurazon, picolinafen|
|G||acifluorfen, butafenacil, carfentrazone, flumioxazin, oxyfluorfen, pyraflufen|
|H||benzofenap, pyrasulfotole, isoxaflutole|
|I||2,4-D, clopyralid, dicamba, MCPA, mecoprop, picloram, triclopyr|
|J||2,2–DPA, flupropanate, molinate, prosulfocarb|
|K||napropamide, dimethenamid, metolachlor, propachlor|
|Z||Flamprop, endothal, DSMA|
In Australia, the letters (A, B, C etc) are used to identify the different Mode of Action groups whereas overseas, the numbers (1, 2, 3 etc) are used.
Unfortunately, if a weed becomes resistant to a herbicide, it often becomes resistant to other herbicides in the same Mode of Action group. Sometimes, it can even become resistant to all other herbicides in the same group.
It is also possible for a weed to become resistant to herbicides from more than one Mode of Action group. This is called 'multiple herbicide resistance' and is very, very difficult to manage.
A key method for managing resistance is keeping chemical use records, which can be used to monitor what Modes of Action have been used. It is compulsory to make specified records within 48 hours of using an agricultural chemical product, and keep these records for a period of two years. This applies to all agricultural chemicals used, including poison baits used for pest animal control. This requirement came into effect on 24 July 2007 and excludes the use of household or home garden products.
An example of herbicide resistance is Annual Ryegrass (Lolium rigidum), found in broadacre cropping areas of Victoria. Annual Ryegrass is frequently found to be resistant to some or all Group A herbicides. This means that careful selection of herbicides from different Mode of Action groups is required to achieve effective chemical control of this weed. Chemical control alone is not a long term answer.
There have also been several documented cases of glyphosate resistance in annual ryegrass and more recently, in barnyard grass.
Integrated Weed Management (IWM)
To ensure sustainable weed control, Integrated Weed Management (IWM) should to be implemented. IWM involves the use of a range of different strategies against the weed, not just chemicals.
Other IWM strategies available include:
- Physical control
- Cultural (management) control
- Genetic control
- Biological control
- Australian Pesticides and Veterinary Medicines Authority website
- CropLife Australia website
- The Department's Chemical Use website
DEPI Chemical Standards Officers
Fax: 03 5430 4590
|Steve Field||(03) 5430 4463|
|Alex Perera||(03) 5430 4591|
|Felicity Collins||(03) 5833 5203|
|Neil Harrison||(03) 5336 6616|
|Jane Rhodes||(03) 5147 0832|
Enquiries from other regions should be directed to the nearest of the above-named regional officers.
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