The “mode of action” is the biological process or enzyme that the herbicide interrupts, affecting normal plant growth and development. For example 2, 4-D is a growth regulator mode of action herbicide that affects auxin growth. The main mechanism seems to be through pumping the herbicide into the cell vacuole. As this involves specific transporters for the herbicide, resistance usually occurs to a single herbicide only. The mode of action is the way in which the herbicide controls susceptible plants. It usually describes the biological process or enzyme in the plant that the herbicide interrupts, affecting normal plant growth and development. In other cases, the mode of action may be a general description of the injury symptoms seen on susceptible plants. In Oklahoma crop production, 11 different herbicide modes of action are commonly used, and each is unique in the way it controls susceptible plants. Some herbicide modes of action comprise several chemical families that vary slightly in their chemical composition, but control susceptible plants in the same way and cause similar injury symptoms. Herbicides can also be classified by their “site of action,” or the specific biochemical site that is affected by the herbicide. The site of action is a more precise description of the herbicide’s activity; however, the terms “site of action” and “mode of action” are often used interchangeably to describe different groups of herbicides. Knowing and understanding each herbicide’s mode of action is an important step in selecting the proper herbicide for each crop, diagnosing herbicide injury, and designing a successful weed management program for your production system. Over-reliance on a single herbicide active ingredient or mode of action places heavy selection pressure on a weed population and may eventually select for resistant individuals. Over time, the resistant individuals will multiply and become the dominant weeds in the field, resulting in herbicides that are no longer effective for weed control. Simply rotating herbicide active ingredients is not enough to prevent the development of herbicide-resistant weeds. Rotating herbicide modes of action, along with other weed control methods, is necessary to prevent or delay herbicide-resistant weeds. Always read each product’s label to determine the mode of action and best management practices for herbicide-resistant weeds. Many weeds have developed “cross resistance” and are resistant to multiple herbicides within a single mode of action. Most waterhemp populations in Oklahoma, for example, are cross-resistant to both Scepter (chemical family: imidazolinone) and Classic (chemical family: sulfonylurea). Both of these herbicides are ALS inhibitors, but belong to different chemical families within the same mode of action. Therefore, it is important to not only rotate herbicide active ingredients but also to rotate modes of action to prevent herbicide-resistance weed populations.

1. Herbicide Modes of Action

2. Classification by Mode of Action
1) Photosynthesis inhibitors
2) Plant growth regulators
3) Amino acid biosysthesis inhibitors
4) Growth inhibitors
5) Pigment inhibitors
6) Grass specific herbicides
7) Membrane disrupters

3. Remember…
 Photosynthesis (food)
 Respiration (energy)
 Amino acids (proteins/growth)
 Lipids (cell membranes)
 Pigments (energy/light capture)
• Chlorophyll, carotenoids
 Mitosis (cell division)

4. Mode of Action
 The sequence of events that leads to plant
death or growth interruption OR Sequence
of events from absorption into the plant
until the plant dies.
 2 phases
* movement to target site
* interaction at target site

5. Mechanism of Action (Site)
 Location at which a herbicide exerts
its toxicity at the cellular level
 more specific

6. Types of Herbicides
 Herbicides work to reduce weeds through many
mechanisms, but all serve to disrupt weed growth.
 Growth regulators diminish cell division and enlargement
and are used largely to kill broadleaf weeds.
 Pigment inhibitors break down chlorophyll, which is
necessary for photosynthesis.
 Seedling growth inhibitors work by inhibiting plant growth
just after germination, interfering with the growth of
roots/shoots.
 Other herbicides work by inhibiting the production of
materials necessary for plant growth (amino acids & lipids).

7. Callus tissue— A mass of plant cells that form at a
wounded surface.
Chlorosis— A yellowing in plant color due to a decline
in chlorophyll levels.
Epinasty— A bending of plant parts (e.g., stems of leaf
petioles) downwards due to increased growth on the
upper side of an affected plant part. Often associated
with the plant growth regulator herbicides.
Necrosis— The death of specific plant tissue while the
rest of the plant is still alive. Necrotic areas are generally
dark brown in color.

8. Photosynthetic inhibitors
Biochemically speaking, photosynthesis is a fairly
complicated process that takes place within plant
cells and requires many enzymes and the transfer
of electrons. If any of these photosynthetic systems
is disrupted for any reason, the process will shut
down and the plant will die.

9. How Photosynthesis Inhibitors Work
Photosynthesis is driven largely by the transfer of
electrons from chlorophyll molecules into the surrounding
cytochromes.
These electrons are passed along a series of cytochromes
in what is known as an electron transport system.
Sunlight activates these electrons where they are passed
along another electron transport chain and are eventually
used in a carbon-fixing reaction.
PIH work by blocking the transfer of electrons.
Without electron transfer, energy from the sun cannot be
transformed into energy that is usable by plants to generate
new tissue and sustain life.

10. Photosynthetic Inhibitor Uses
Inhibitors of photosynthesis are used mainly to
control broad-leaved weeds. That is, grass crops
such as corn benefit the most from PI.
Symptoms of Photosynthesis Inhibitors
Plants that have been exposed to PI herbicides
will begin to appear yellow on the veins and
around the edges of the oldest leaves, which will
be followed by similar damage to younger
leaves. Yellow spots may also appear on affected
leaves.

11. Photosystem -I Inhibitors
 Accept electrons from PSI to form
radicals
 Super radicals formed to create peroxides
 Diquat, paraquat

12. Photosystem -II Inhibitors
 Inhibit photosynthesis by binding to QB-
binding niche on D1 protein
 Atrazine, Basagran, Buctril, Sencor,
Simazine

13. Paraquat

14. Range and pasture herbicide MOA
 Plant growth regulators
 Amino acid biosynthesis inhibitors

15. Plant Growth Regulators
 Referred to as synthetic auxins (regulate growth)
 Translocate in both xylem and phloem.
 Can act at multiple sites in a plant to disrupt hormone
balance and protein synthesis
 Abnormal growth resulting in twisting stems
 Stems swelling due to rapid cell division & accumulation
at growing points
 Grasses are not susceptible (may be due to differences in
vascular tissue structure or differences in translocation
or metabolism)
(Tordon, Redeem, Banvel, 2,4-D)

16. Common Leaf Symptoms from PGR Exposure
normal
cupped and blistered from
PGR exposure

17. short internode
accumulation
In new growth
Foliar PGR Application

18. callus formation on roots
translocation to
growing point
swollen
hypocotyl
lack of root
development
Root Absorption of Plant Growth Regulator
Herbicides

19. Amino Acid Inhibitors
 Prevent synthesis of certain amino acids produced
by plants but not animals.
 Excellent foliar and root absorption
 Broad weed spectrum
 Translocates to shoot and root new growth
 Plants stop growing shortly after application
 Glyphosate, Escort, Roundup)
 Roundup introduced 1971
 Sulfonylurea introduced in 1979

20. ALS Inhibitors
 Inhibit acetolactate synthase (ALS) enzyme
 enzyme needed to produce certain amino
acids (isoleucine, leucine, valine)
Commonly Used ALS Herbicides
Classic, Exceed, Express, Glean, Harmony

21. Glyphosate (Roundup) Drift
chlorosis
shortened
internodes
stem proliferation

22. Aryloxyphenoxypropionates & Cyclohexanediones.
Site of Action Group 1 - Inhibitors of acetyl CoA
carboxylase (ACCase) also known as "Grass
Growing Point Disintegrators“
These herbicides prevent the formation of fatty
acids, components essential for the production of
plant lipids.
Broadleaf plants are tolerant to these herbicide
families, however, almost all perennial and annual
grasses are susceptible.
Lipid Synthesis (ACCase) Inhibitors

23. ACCase Inhibitors
 Inhibit acetyl-CoA-carboxylase (ACCase) enzyme
 Enzyme needed for fatty acid synthesis
 Dim’s and Fop’s
 Achieve, Assure, Fusilade, Poast, Select
 Plant Injury Symptoms
 Injury symptoms are slow to develop (7 to 14 days)
and appear first on new leaves emerging from the
whorl of the grass plant. These herbicides are taken
up by the foliage and move in the phloem to areas
of new growth.

24. “rotted” meristem

25. Pigment Inhibitor
Pigment inhibitors prevent plants from forming
photosynthetic pigments.
As a result, the affected plant parts become white to
clear.
Command a soil-applied herbicide, is the only member of
this family in use at this time.
Command is taken up by plant roots and shoots and can
move in the xylem to plant leaves. The newly developed
foliage of many plant species is so sensitive to Command
that very small amounts can whiten new plant growth.

26. Pigment Inhibitors (Bleaching Herbicides)
 Inhibitors of carotenoid biosynthesis,
phytoene desaturase (PDS) and
hydroxyphenyl pyruvate dioxygenase
(HPPD)

27. Mitosis Inhibitors
 Microtubule inhibition
• Treflan, Prowl, Sonalan, Surflan,
Dacthal

28. Dual Injury