Herbicides and their Modes of action

Phenyl pyridazinones

-pigment inhibitor

-norfulurazon (representative herbicide)

isoxazolidones

-pigment inhibitor

-clomazone (representative herbicide)

triketones

-pigment inhibitor

-mesotrione (representative herbicide)

pigment inhibitors mechanism of action

inhibits specific enzyme in the pathway to creating pigments such as carotenoids, xanthophylls, and pre-products for chlorophyl

clomazone’s mechanism of action

inhibits DOXP synthase

norflurazon’s mechanism of action

inhibits phytoene desaturase

fluridone’s mechanism of action

a pigment inhibitor that inhibits zeta-carotene desaturase

mesotrione’s mechanism of action

inhibits HPPD

mode of action for pigment inhibitors

1. Uptake and translocation to chloroplast (thylakoid membrane)
2. Inhibits specific enzyme
3. Carotenoids and xanthophylls no longer made
4. Photosynthesis in new tissue stops
5. ROS generated are not quenched (plant still in light)
6. Cells die
7. Plants die

fops

-lipid synthesis inhibitor

-fluazifop (representative herbicide)

dims

-lipid synthesis inhibitor

-clethodim (representative herbicide)

lipid synthesis inhibitor mechanism of action

inhibits acetyl coenzyme A carboxylase (ACCase)

lipid synthesis inhibitor mode of action

1. Uptake and translocation to chloroplast (thylakoid membrane)
2. Inhibits ACCase
3. Lipid synthesis stops
4. Plant growing point dies
5. Plants die

fops and dims effect on plants

-effective against monocots

-not effective against broadleaves, lilies, and sedges

why are fops and dims ineffective against broadleaves, sedges, and lilies?

grasses have a eukaryotic version of the chloroplast while broadleaves, lillies, and sedges have the prokaryotic form of chloroplast

what happens to the plant once ACCase is stopped?

the plant can’t make lipids or waxy cuticles or suberin, or cutin, or membranes.

key symptoms of lipid inhibitors

necrosis of meristematic tissue, sometimes spots on leaves

phenoxy carboxylic

-growth regulator

-2,4-D (representative herbicide)

symptoms of 2,4-D

youngest leaves curl upwards,

leaves appeared strapped (feathering on veins),

petioles and stemps twisted in circular motion (epinasty)

stems can be brittle

pyridine carboxylic acids

-growth regulator

-tryclopyr (representative herbicide)

dicamba

-growth regulator

-dicamba

mechanism of 2,4-D

mimics auxin

plant response to auxin mimicing herbicides

1. growth stimulation phase

   occurs within hours

   activates ethylene synthesis

   accumulation of ABA

   abnormal growth

2. growth inhibition phase

   occurs within 24 hours

   strong growth inhibition of root and shoot meristem

   stomates close

   ROS asimilation

3. Senescence and tissue decay phase

   accelerated leaf senscence

   chloroplast damage (ROS) and chlorosis

   Vascular system collapses

   plant dies

growth regulator mechanism of action

bind to auxin and stimulate growth process

growth regulator mechanism of action

1. Uptake and translocation to membranes and nucleus in meristematic cells
2. Bind to ABP’s and stimulate growth processes
3. Loosen cells walls, deforming stems and petioles
4. Turn on gene expression, ethylene, and ABA synthesis, ROS production
5. Vascular tissue collapses
6.Plants die

seedling growth inhibitors otherwise known as mitotic disrupters

affect the plants ability to perform mitosis correctly by tampering with the microtubules used in mitosis and meiosis

family dinitroanalines

-mitotic disrupter

-trifluraline (representative herbicide)

family dithiopyr

-mitotic disrupter

-dithiopyr

symptoms of trifluralin and dithiopyr

stunted plants with thick stubby roots, grass roots may be stubby and red in color

spindle microtubules

assist chromosomes to line up in the middle of cell and move them to opposite poles

phragmoplast microtubules

assist formation of cell walls to form daughter cells

cortical microtubules

assist in cell elongation

what do dinitroanilines do in the plant

they block the assembly of microtubules

what happens when plants try to elongate without microtubules

they become isodiametric eg. squarish round

mitotic disrupter mechanism of action

herbicides bind to tubulin and inhibit the formation of microtubules

mitotic disrupter mode of action

1. Uptake and translocation to meristematic cells
2. Microtubule formation stops
3. Cell division and elongation stops
4. New cells only grow isodiametrically
5. Root, shoot (coleoptile, hypocotyl) growth stops
6. Uptake of water and nutrients disrupted
7. Plants die

essential amino acids for plants

isoleucine, leucine, phenylalanine, tryptophan, valine

conditionally essential

glutamine, tyrosine

what pathway does glyphosate block

shikimic acid pathway

what does the shikimic acid pathway do

creates 30 percent of the plants dry weight

creates tyrosine, phenylaline, and tryptophan

glyphosate mechanism of action

binds to ESPS synthase

glyphosate mode of action

1. Uptake and translocation to chloroplast
2. Inhibition of EPSPs activity
3. Plant growth stops immediately
4. Growing points (meristematic tissue) die
5. Plants die

characteristics of glyphosate

1. Accumulation in meristems; systemic
2. Effects annuals, biennials, perennials
3. Highly water soluble (surfactants important)
• Entry into plants in drought stress challenging
4. High Kd value so tight adsorption to soil
5. Only has POST activity
6. Most widely used herbicide in the world

“all substances are poisons, there is none that is not a poison. the right dose differentiates a poison from a remedy”

Paracelsus (1493-1541)

sulfonylureas

-amino acid inhibitor

-chlorimuron ethyl (representative herbicide)

imidazolinones

-amino acid inhibitor

-imazethapyr representative herbicide

what is the most numerous herbicide that also needs just ounces instead of pounds

chlorimuron-ethyl

which herbicides inhibit ALS

sulfonylureas and imidazolinones

mechanism of sulfonylureas and imidazolinones

bind to ALS

mode of sulfonylureas and imidazolinones

1. Uptake and translocation to chloroplast
2. Inhibition of ALS activity
3. Plant growth stops immediately
4. Growing points (meristematic tissue) die
5. Plants die
Notice that no toxins are made; plant runs out of energy

origin of glufosinate

started out as a bacteria bi-product that was found to be useful as an herbicide

glufosinate mechanism of action

binds to glutamine synthatase stopping the production of glutamine

glufosinate mode of action

1. Uptake and translocation to chloroplast
2. Inhibition of glutamine synthetase
3. Chloroplasts accumulate high levels of NH3
4. Feedback inhibition of photorespiration and Calvin cycle
5. Photosynthesis stops and light energy given to O2 to
generate ROS
6. Autocatalytic lipid peroxidation ensues; cells die
7. Plants die

crops resistant to glufosinate

corn

soybeans

cotton

canola

key symptom of glufosinate

green halo around the necrotic lesions

what is glutamine

a precurser for 4 amino acids when it can’t be made extra ammonia gets into the plant.