Resistance groups
The number that matters most.
The group on the label tells you how a product kills. Spray the same group year after year and you are selecting for the weeds it can't kill.
of tested Saskatchewan fields had Group 2 resistant cleavers.
of kochia tested in Alberta was glyphosate resistant.
of fields in a recent Manitoba survey had wild oats with Group 1 and 2 resistance.
Figures from Prairie weed surveys, as reported by Top Crop Manager and The Western Producer. Exact results vary by survey and year.
Rotation check
What did you spray last year?
Pick the herbicide groups you relied on. It shows what's left on this list that works a different way.
Pick a group above to start.
Herbicides
-
ACCase inhibitors
FOPs, DIMs and DENs
Shuts down the enzyme grass plants use to build fat for new cell membranes.
Grass weeds stop growing within days, the growing point rots out, and the plant dies over a couple of weeks.
Group 1 resistant wild oats are common across the Prairies. Different chemical families in the group are not always interchangeable.
-
ALS / AHAS inhibitors
SUs, IMIs, TPs and SCTs
Blocks the enzyme that makes three key amino acids, so the plant can no longer build protein.
Growth stops first. Yellowing and death come slowly, sometimes over weeks.
The most resistance-prone group on the Prairies. Kochia, wild oats, cleavers and many others have Group 2 resistant biotypes.
-
Microtubule inhibitors
Dinitroanilines
Stops cells dividing properly in germinating roots and shoots.
Weeds die as they germinate in treated soil. Roots look short and clubbed.
Needs to be in the soil. Check the label for incorporation and soil-moisture requirements.
-
Synthetic auxins
Phenoxys, benzoics, pyridines and quinolines
Mimics a natural plant hormone, overloading the growth system.
Broadleaf weeds twist, curl and grow themselves to death.
Group 4 resistant kochia has been confirmed on the Prairies. Keep drift and sprayer clean-out in mind around sensitive crops.
-
Photosystem II inhibitors
Triazinones
Binds in the chloroplast and stops photosynthesis at photosystem II.
Leaves yellow from the edges in, then die.
Soil type and organic matter can affect both weed control and crop safety.
-
Photosystem II inhibitors
Nitriles and benzothiadiazoles
Stops photosynthesis at a different spot on photosystem II from Group 5.
A fast contact burn on the leaves it hits.
Contact activity means coverage matters.
-
EPSP synthase inhibitors
Glycines
Blocks the shikimate pathway, which plants use to make essential amino acids.
Moves all through the plant, roots included. Slow but thorough.
Glyphosate-resistant kochia is widespread on the Prairies, so tank-mix partners from other groups matter.
-
Glutamine synthetase inhibitors
Phosphinic acids
Blocks the enzyme plants use to deal with ammonia, which then builds up to toxic levels.
A contact burn, visible within days.
Water volume and coverage matter, because it does not move far in the plant.
-
DOXP synthase inhibitors
Isoxazolidinones
Stops the plant making carotenoids, the pigments that protect chlorophyll.
Weeds come up bleached white, then die.
Can move off target as vapour. Check the label on buffer zones and application.
-
PPO inhibitors
Triazolinones, pyrimidinediones, N-phenylimides and phenylpyrazoles
Triggers a reaction that ruptures cell membranes in sunlight.
Very fast burn, often visible within a day.
Popular as a burnoff partner because it brings a second group against glyphosate-resistant kochia.
-
VLCFA inhibitors
Thiocarbamates, chloroacetamides and isoxazolines
Stops the very long fatty acids a germinating shoot needs.
Weeds die in the soil as they try to emerge.
It will not control weeds that are already up. Older labels may still call the thiocarbamates Group 8.
-
Photosystem I electron diverters
Bipyridyliums
Steals electrons at photosystem I and creates compounds that destroy cell membranes.
Leaves and stems dry down very quickly in sunlight.
A true contact product. It does not move to the roots, so it will not kill perennials.
-
HPPD inhibitors
Pyrazoles and triketones
Blocks the HPPD enzyme, which cuts off the pigments that shield chlorophyll from sunlight.
New growth turns bleached white, then the tissue dies.
On the Prairies it is usually sold with bromoxynil, which puts Groups 6 and 27 in one product.
Fungicides
-
MBC fungicides
Benzimidazoles
Binds tubulin in the fungal cell, so the cell cannot divide.
Holds back fungi on and around treated seed.
A single-site mode of action with a long resistance history, so it is normally blended with other groups.
-
DMI (triazoles)
Triazoles and triazolinthiones
Stops fungi making sterols for their cell membranes.
Moves into the leaf and locally upward with the water stream.
Rotate or combine with other FRAC groups to protect it from resistance.
-
Phenylamides
Acylalanines
Blocks RNA production in water moulds such as Pythium.
Protects germinating seed against seed rots.
Narrow spectrum, so usually paired with other seed-treatment actives.
-
SDHI
Carboxamides
Blocks energy production in the fungus at complex II of the mitochondria.
Stops spores germinating and fungi growing.
A single-site mode of action, so stewardship matters.
-
QoI (strobilurins)
Strobilurins
Blocks energy production in the fungus at complex III of the mitochondria.
Strongest as a preventive, before disease is established.
A resistance-prone group. Avoid back-to-back use.
-
Osmotic signal disruptors
Phenylpyrroles
Interferes with the signalling fungi use to manage water pressure in their cells.
Stops spores germinating and fungal threads growing on the seed and in the soil around it.
Mostly used on seed in blends, where it covers a different target from the other actives.
-
Multi-site contact fungicides
Dithiocarbamates
Attacks many enzymes in the fungus at once.
Sits on the leaf as a protective coat and does not move in the plant.
Hitting many sites keeps resistance risk low, but rain can wear it off and new growth is not protected.
-
Multi-site contact fungicides
Chloronitriles
Ties up many enzymes in the fungus at once.
Sits on the leaf as a protective coat and does not move in the plant.
Hitting many sites keeps resistance risk low, but it has to be on before infection.
Insecticides
-
Acetylcholinesterase inhibitors
Organophosphates
Blocks the enzyme that clears nerve signals, so nerves keep firing.
Fast knockdown of the insects it reaches.
Organophosphates carry strict handling and re-entry rules, and they are hard on bees. Read the label first.
-
Nicotinic receptor modulators
Neonicotinoids
Binds the nerve receptors insects use to pass signals.
Moves from the seed into the seedling, so pests feeding early take it in.
The main seed-treatment tool on the Prairies. Follow the label on seed handling and dust around pollinators.
-
Ryanodine receptor modulators
Diamides
Forces calcium out of storage in insect muscle, so the muscles lock up.
Insects stop feeding quickly, then die over the next few days.
Strongest on chewing pests. Rotate groups to protect it from resistance.
-
Sodium channel modulators
Pyrethroids
Holds nerve sodium channels open, so nerves keep firing.
Fast knockdown of insects it contacts or that eat treated leaves.
Broad spectrum, so it also hits beneficial insects. Cool temperatures often improve pyrethroid activity, heat can reduce it.