Herbicide selectivity and modes of action
How herbicides kill weeds but spare crops, the HRAC mode-of-action groups with examples, safeners, herbicide-tolerant crops, and a spray dose sum.
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A herbicide sprayed over a wheat field kills wild oats and broadleaf weeds but leaves the wheat green. A different herbicide, sprayed on a fence line, kills everything. The first is selective, the second non-selective, and understanding why is the key to using herbicides safely and effectively.
Herbicide selectivity and modes of action are core topics in weed science, agronomy and plant protection exams, and they matter in practice because choosing and rotating modes of action is the main defence against herbicide-resistant weeds.
Ways to classify herbicides
- By selectivity: selective (kill some plants, spare others) or non-selective (kill most green plants).
- By timing: pre-plant incorporated, pre-emergence (applied to soil before weeds emerge) or post-emergence (applied to growing weeds).
- By movement in the plant: contact herbicides kill only the tissue they touch; systemic (translocated) herbicides move through the xylem, phloem or both to growing points and roots.
- By chemical family, such as triazines, sulfonylureas or phenoxy acids.
- By mode of action: the plant process the herbicide disrupts. This is the most useful classification for resistance management.
How selectivity works
Selectivity is relative, not absolute: at a high enough dose almost any herbicide injures the crop. It comes from differences in where the herbicide ends up and how the plant handles it.
Selectivity by position and timing
- Depth protection: a pre-emergence herbicide that stays in the top few centimetres of soil kills small-seeded weeds germinating there, while a large crop seed sown deeper escapes.
- Directed and shielded sprays: spraying under the canopy of a tall crop or between rows.
- Timing: non-selective herbicides used before crop emergence, or before planting, to kill an existing flush of weeds.
Selectivity by the plant
- Uptake: leaf shape, angle, wax and hairs change how much spray is retained and absorbed; grasses with upright, narrow leaves often retain less than broadleaf weeds.
- Translocation: differences in how much herbicide reaches growing points.
- Metabolism: the most important mechanism. Tolerant crops rapidly convert the herbicide into inactive products. Maize detoxifies atrazine mainly by conjugation with glutathione; rice breaks down propanil quickly using an enzyme (aryl acylamidase) that barnyard grass has in much smaller amounts; wheat metabolises several grass herbicides that kill wild oats.
- Target site: the crop has a form of the target enzyme that the herbicide binds weakly. Broadleaf crops tolerate ACCase herbicides because their plastid ACCase differs from that of grasses.
- Safeners: chemicals added to the product that switch on the crop's own detoxification enzymes without protecting the weed, such as cloquintocet-mexyl with clodinafop in wheat, or fenclorim with pretilachlor in rice.
Herbicide-tolerant crops
Selectivity can also be built into the crop:
- Genetic modification: crops carrying a tolerant EPSPS enzyme survive glyphosate; crops with the pat or bar gene detoxify glufosinate; others tolerate 2,4-D or dicamba.
- Conventional breeding and mutagenesis: imidazolinone-tolerant crops, such as several rice, wheat, sunflower and canola varieties, carry a mutated ALS enzyme.
These make broad-spectrum herbicides selective, but heavy reliance on a single herbicide has selected for resistant weeds, of which glyphosate-resistant Palmer amaranth is the best-known example.
The modes of action
The Herbicide Resistance Action Committee (HRAC), together with the Weed Science Society of America, groups herbicides by mode of action. In 2020 HRAC moved to a single numeric code shared worldwide; the older letter codes still appear in many textbooks.
| HRAC group (old letter) | Mode of action | Examples | Notes |
|---|---|---|---|
| 1 (A) | ACCase inhibitors (lipid synthesis) | clodinafop, fenoxaprop, clethodim, pinoxaden | kill grasses; broadleaf crops tolerant |
| 2 (B) | ALS (AHAS) inhibitors (branched-chain amino acids) | metsulfuron, chlorsulfuron, imazethapyr, bispyribac | very low doses; resistance common |
| 3 (K1) | microtubule assembly inhibitors | pendimethalin, trifluralin | pre-emergence, small-seeded weeds |
| 4 (O) | synthetic auxins | 2,4-D, MCPA, dicamba, clopyralid | broadleaf weeds in cereals and grass |
| 5 (C1, C2) | photosystem II inhibitors | atrazine, metribuzin, diuron, isoproturon | many pre-emergence uses |
| 6 (C3) | photosystem II inhibitors (different binding) | bromoxynil, bentazon | contact, post-emergence |
| 9 (G) | EPSPS inhibitor (aromatic amino acids) | glyphosate | non-selective, systemic |
| 10 (H) | glutamine synthetase inhibitor | glufosinate | non-selective, mostly contact |
| 12 (F1) | phytoene desaturase inhibitors (pigments) | diflufenican, norflurazon | bleaching |
| 14 (E) | PPO inhibitors | oxyfluorfen, fomesafen, carfentrazone | fast-acting, contact |
| 15 (K3) | very-long-chain fatty acid inhibitors | metolachlor, pretilachlor, butachlor | pre-emergence grass control |
| 22 (D) | photosystem I electron diverters | paraquat, diquat | non-selective contact; highly toxic to people |
| 27 (F2) | HPPD inhibitors (pigments) | mesotrione, topramezone, isoxaflutole | bleaching, maize |
| 29 (L) | cellulose synthesis inhibitors | indaziflam, isoxaben | pre-emergence |
Product labels in many countries show the group number, so farmers can rotate and mix groups without needing to know the chemistry. Paraquat is banned or restricted in many countries because of its acute toxicity.
Using selectivity well
- Follow the label for crop, growth stage, dose and timing; selectivity often holds only within a crop stage window.
- Avoid stress conditions: crops under drought, frost or waterlogging metabolise herbicides more slowly and are more easily injured.
- Mind the soil: pre-emergence herbicides are more active and less selective on light, low-organic-matter soils, so rates are often lower there.
- Check rotation restrictions: persistent herbicides, such as some ALS inhibitors and auxins, can injure the next crop.
- Rotate and mix modes of action, and combine herbicides with cultural and mechanical control.
Working out a herbicide dose
A recommendation is pendimethalin at 1.0 kg of active ingredient per hectare, pre-emergence, in 500 L of water per hectare. The product contains 330 g of pendimethalin per litre.
- Product per hectare = 1,000 g ÷ 330 g/L ≈ 3.0 L/ha.
- With a 16 L knapsack sprayer, one tank covers 16 ÷ 500 = 0.032 ha, or 320 m2.
- Product per tank = 3.0 L × 0.032 ≈ 0.097 L, about 97 mL.
- For a 0.4 ha field: 0.4 × 3.0 = 1.2 L of product in 200 L of water, about 12.5 tanks.
The sprayer must first be calibrated so that it really delivers 500 L/ha at the operator's walking speed.
Key points
- Herbicides are classified by selectivity, timing, movement (contact or systemic), chemistry and mode of action.
- Selectivity comes from position (depth, directed spray, timing) and from the plant (uptake, translocation, metabolism, target site), helped by safeners.
- Metabolism is the main basis of crop tolerance, for example atrazine in maize and propanil in rice.
- Herbicide-tolerant crops, from genetic modification or mutagenesis, make broad-spectrum herbicides selective.
- HRAC numeric groups (1 ACCase, 2 ALS, 3 microtubules, 4 auxins, 5 and 6 PSII, 9 EPSPS, 10 GS, 14 PPO, 15 VLCFA, 22 PSI, 27 HPPD) guide mode-of-action rotation.
- Product dose = active ingredient rate ÷ concentration.
What the exams ask
- School-leaving and entrance papers: selective and non-selective, pre- and post-emergence, and examples of herbicides for major crops.
- Degree and research-fellowship entrances: mechanisms of selectivity, modes of action and HRAC groups, safeners, herbicide-tolerant crops, and dose calculations.
- Professional examinations: herbicide resistance management, rotation restrictions, and choosing herbicides for weed spectra and crop stages.
Described in general terms: the kind of examination, not a past paper. Laisha never reproduces exam questions.
Questions people ask
Why does 2,4-D kill broadleaf weeds but not wheat?
Grasses absorb and move less of it, metabolise it faster, and have protected growing points and a different vascular arrangement. At the wrong growth stage or dose, cereals can still be injured.
What does a safener do?
It triggers the crop to produce more detoxifying enzymes, so the crop breaks the herbicide down before it causes harm. It does not protect the weeds, which respond little.
Why do labels list a group number?
So users can rotate or mix herbicides with different modes of action, which slows the evolution of resistant weeds.
Sources
- Herbicide Resistance Action Committee. HRAC Mode of Action Classification (2024 update). HRAC Global, online.
- Monaco, T. J., Weller, S. C. and Ashton, F. M. Weed Science: Principles and Practices, 4th edition. Wiley, 2002.
- Davies, J. and Caseley, J. C. "Herbicide safeners: a review." Pesticide Science 55, 1043–1058 (1999).
- Heap, I. The International Herbicide-Resistant Weed Database. Online, www.weedscience.org.
- Shaner, D. L. (ed.) Herbicide Handbook, 10th edition. Weed Science Society of America, 2014.
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