Lecture notes on Weed Management

1. MODE OF ACTION AND MECHENISM OF ACTION
OF HERBICIDES
Prepared By: Dr. Pooja Goswami
College of Agriculture, Balaghat COA, Balaghat

2. Mode of action of herbicide refers to the entire chains/sequences of
events occurring from the first contact of the herbicides to the plant to
its ultimate/final effect, which could be death of a plant. It, therefore,
comprises of sum total of anatomical, physiological and biochemical
responses that bring about the total phototoxic action in plants
Mechanism of action
Mechanism of action, however, refers to the particular biochemical
and physiological reactions, which bring about the ultimate
herbicidal effect.
Mode of action of herbicide
COA, Balaghat

3. APPLICATION
Uptake Root or leaf cuticle penetration
Transport Xylem or phloem conduction
Metabolism
Biochemical degradation,
Binding or degradation
TARGET SITE
Organelles
Chloroplast
Ribosome
Accumulation of potentially toxic
dose
Action
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4. Mode of action herbicide includes
1) Herbicide absorption/penetration/uptake
i) Foliar absorption
ii) Root absorption
2) Herbicide translocation in plants
i) Symplastic movement
ii) Apoplastic movement
3) Mechanism of action
i) Cell division inhibition
ii) Cell elongation inhibition
iii) Photosynthesis inhibition
iv) Respiration inhibitors
v) Nucleic acid, amino acid and protein biosynthesis
inhibition
vi) Membrane function disruption
vii) Lipid biosynthesis inhibition
COA, Balaghat

5. COA, Balaghat
Symplastic movement
 Herbicides move through phloem with sugars or photosynthates
produced during photosynthesis and get accumulated where sugars are
being used or stored.
 Symplastic movement is usually more applicable to post-emergence
foliage – active, systemic herbicides, viz., glyphosate, fenoxaprop- p-
ethyl, 2,4-D etc.
Apoplastic movement
 In apoplastic movement, the herbicides are primarily absorbed by roots
and move through xylem in plants and translocated along with water or
mineral nutrient ions.
 Apoplastic movement is usually more applicable to pre-plant or pre-
emergence soil-applied, systemic herbicides, e.g. atrazine, isoproturon,
pendimethalin, fluchloralin etc.

7. S.No. Chemical groups Members
1. Acetamides (amides) Diphenamid, napropamides, isoxaben
Acetamides (anilides) Propanil, acetachlor, alachlor, butachlor
2. Phenoxy alkanoic
acid
2,4-D,MCPB, 2,4-DB,MCPA, 2,4,5-T
3. Benzoic acids 2,3,6-TBA, dicamba, chloramben
4. Benzonitriles/nitriles Bromoxynil, ioxynil
5. Bipyridiliums Diquat, paraquat
6. Carbamates &
thiocarbamates
Asulam, metham, chloropropham, biallate,
triallate, benthiocarb
7. Cyclohexanediones Alloxydim, sethoxydim
8. Dinitroanilines Fluchloralin, pendimethalin, oryzalin,
trifluralin
9. Diphenylethers Nitrofen, aciflurofen, oxyflurofen, lactofen
10. Dinitrophenols DNOC, Dinoseb, dinosam
11. Imidazolinones Imazamethabenz, imazethapyr, imazaquin

8. 12 Aryloxy phenoxy
propionates
Diclofop-methyl, fenoxaprop-p-
methyl, quizalofop-p-ethyl
13 Phenylureas Isoproturon, monuron, linron,
methabenzthiazuron
14 Organophosphorus Glyphosate, gluphosinate,
anilophos
15 Triazines Atrazine, simazine, cynazine,
metribuzin
16 Sulfonylureas Sulfosulfuron, chlorsulfuron,
metsulfuron-methyl
17 Uracils Bromacil, lenacil
18 Heterocyclic
compounds
Pyrazon, Clopyralid,
triclopyr,fluoroxypyr
19 Aliphatic acids MCA, TCA

9. Chemical structure:
2,4 – [ Dichlorophenoxy ] acetic acid
O—CH2—C—OH
O
Cl
Cl
2,4 – D acid
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10. O—CH2—CH2—CH2—C—OH
O
Cl
Cl
2,4 – DB acid (2,4 - dichlorophenoxy) butyric acid
O—CH2—CH2—CH2—C—O
O
Cl
Cl
Salt
CH3
NH2
CH3
+
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11. O—CH2—CH2—CH2—C—OH
O
CH3
Cl
4 (4 – Chloro-2- methylphenoxy) butanoic acid
MCPB –acid
O—CH2—CH2—CH2—C—O
O
CH3
Cl
+ Na+
MCPB – sodium salt
COA, Balaghat

12. COA, Balaghat
Herbicides of this group absorbed by the broad-leaved plants via
roots and foliage.
Plant roots absorb polar (salt) forms of 2, 4-D more readily than ester
form of 2, 4-D, whereas the nonpolar (ester) forms more rapidly
penetrate foliage.
A rain-free period of 4 h usually is adequate for uptake and effective
control.
Herbicide is transported primarily via the symplastic pathway
(including the phloem) and accumulates principally at the growing
points of the shoots and root following root uptake.
2, 4-D translocates somewhat in the transpiration stream by the
apoplastic pathway.
Sensitive plants convert salts and ester form into acid form which is
phytotoxic.
Absorption:
Translocation:

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 This group is responsible for excessive cell division and cell
enlargement. Plant cell surrounding vascular tissue undergoes
uncontrolled cell division and cell enlargement which may mechanically
interfere with translocation of food.
 Primary action of these compounds appears to involve cell wall
plasticity and nucleic acid metabolism. 2, 4-D is thought to acidify the
cell wall by stimulating the activity of a membrane bound ATPase-driven
proton pump. The reduction in apoplasmic pH induces cell wall
elongation by increasing the activity of certain enzymes responsible for
cell wall loosening.
 Low concentrations of 2, 4-D also stimulates RNA polymerase, resulting
in subsequent increase in RNA, DNA and protein biosynthesis.
Abnormal increase in these processes presumably leads to
uncontrolled cell division and growth, which results in vascular tissue
destruction.
Mechanism of action:

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 Epinastic bending and twisting of stems and petioles
 Stem swelling (particularly at nodes) and elongation
 Leaf cupping and curling are typical symptoms, when plants
are exposed to these herbicides.
Symptomology

15. 2,4-D metabolism reactions can be divided into two phases:
 Phase-I reaction
1. Hydroxylation(# 4 Cl is displaced by a hydroxyl group and moved to
the # 5 or # 3 carbon).
2. Decarboxylation
 Phase-II reaction
Conjugation with :
• Amino acid (glutamate, aspirate)
• Glucose at the hydroxyl position
2,4-DB metabolism in plant
• B-oxidation
Metabolism in plants:
COA, Balaghat

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17. COA, Balaghat
Mechanism of action
 The most sensitive site of action of the herbicide is on
photosynthesis near photosystem II.
 This involves the blockage of electron transport from QA to QB by
binding to the QB- binding niche on the D1 protein of the PS II
complex in chloroplast thylakoid membranes, this stops CO2 fixation
and production of ATP and NADPH2(all needed for plant growth).
 Blockage of electron transport in photosystem-II leads to the
production of a range of powerful oxidants which damage
membranes, and so on causing rapid destruction of the cell.
Absorption and translocation
 Triazines are rapidly absorbed through roots from soil applications.
 It is exclusively translocated to shoots via the apoplast (including the
xylem).
 Absorption and translocation of triazines from root to shoot is
proportional to amount of water absorbed/transpiration stream.

18. Growth and plant structure:
 They have been shown to inhibit the growth of intact plant and this has
been attributed to blockage of photosynthesis.
 The usual phytotoxic symptoms of the triazine herbicides are interveinal
chlorosis of leaves followed by necrosis.
 Older leaves are more damaged than new growth. Browning of leaf tips
can occur.
 Root growth is not affected.
Metabolism in plants
Glutathione (GSH) conjugation rapidly detoxifies atrazine and simazine
in leaves of tolerant species such as maize and sorghum having high
levels of GSH transferase. It catalyzed formation of S-(4-ethylamino-6-
isopropylamino-S-triazino) glutathione in tolerant species.
COA, Balaghat

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20. Absorption and translocation
 Absorbed rapidly in to foliage, although absorption varies from 20 to 90
percent in 24 hours, root absorption is slower.
 Translocate in both xylem and phloem.
Mechanism of action
 They inhibit acetolactate synthase (ALS), also called acetohydroxy acid
synthase (AHAS), a key enzyme in biosynthesis of the branched chain
amino acids, isoleucine, leucine and valine that are essential in
formation of new cells.
 The two related pathways in which acetolactate is produced from
pyruvate and acetohydroxybutyrate from threonine are catalyzed by a
common enzyme acetolactate synthase (acetohydroxy acid synthase).
 This is effectively inhibited by the sulphonylureas such as chlorsulfuron
and metsulfuron.
COA, Balaghat

21. COA, Balaghat
Pyruvate
AHAS Sulphonylureas
………………………………………………………………………
Acetolactate
Leucine Valine
Site of action of sulpphonylureas
Isoleucine

22. Growth and plant structure
 Growth is inhibited within a few hours after application, but injury
symptoms usually appear after 1 to 2 weeks or more.
 Meristematic areas become chlorotic, followed by a slow general
foliar chlorosis and necrosis.
COA, Balaghat

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24. COA, Balaghat
Absorption and translocation
 Glyphosate is readily absorbed by leaves; little to no glyphosate is
absorbed through the roots under field condition because of microbial
breakdown.
 Primarily translocated in the symplast with accumulation in
underground tissues, immature leaves and meristems.
 Most results suggested little to no apoplastic movement.

25. Aromatic amino acid biosynthesis
Shikimate
Shikimate-3-phosphate
EPSP synthase
5-enolpyruvyl shikimate-3-phosphate
Chorismate
Phenyl alanine Tryptophane Tyrosine
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26. Mechanism of action
 Glyphosate inhibits 5-enolpyruvylshikimate-3-phosphate synthase
(EPSP synthase) enzyme, which catalyzes the biosynthesis of three
aromatic amino acids, namely phenylalanine, tryptophane and tyrosine
in the shikimate pathway.
 Inhibition of this enzyme results in reduced or no production of these
three amino acids, which are highly required for protein biosynthesis.
 These amino acids are also necessary for the production of auxin and
several other secondary plant bio-molecules such as flavonoids,
anthocyanin, alkaloids, which have role in growth regulation and defense
in plant.
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27.  The most common symptoms of glyphosate injury are foliar chlorosis
followed by necrosis.
 Chlorosis may appear first and most pronounced in immature leaves
and growing points.
 Multiple shoots (called a witch’s broom) may develop at the node.
Growth and plant structure
COA, Balaghat

28. Group A Inhibition of fat (lipid) synthesis -ACCase inhibitors
Aryloxy phenoxy propionates, Cyclohexanediones
Group B Inhibition of the enxyme acetolactate synthase – ALS inhibitors
Sulfonylurea, Imidzolinones, Sulfonamides
Group C Inhibition of photosynthesis at photosynthesis II, Triazines, triazines, Ureas,
Nitriles, pyridazinones
Group D Inhibitors of tubulin formation, Dinitroanilines, Benzoic acids
Group E Inhibitors of mitosis, Dinitroanilines, Benzoics acids
Group F Inhibitors of caretenoid biosynthesis, Pyridazonones, Nicotinanilides,
pyridazinones
Group G Inhibitors of protoporphyringen oxidase, Diphenyl ethers, Oxidiazoles
Group H Inhibitors of mitosis, thiocarbates
Group I Disruptors of plant cell growth ,Phenoxy, Benzoic acids, Pyridines
Group J Inhibitors of fat synthesis, Alkanoic acids
Group K Herbicides with multiple sites of action, Carbamates, Amino propionate,
Nitrilies
Group L Inhibitors of photosynthesis at photosystem I, Bipyridylis
Group M Inhibition of EPSP synthase, Glycines
Group N Inhibitors of glutamine synthase ,Glycines
Herbicides mode of action group according to the risk for early
development of resistance
COA, Balaghat

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