Lipid Biosynthesis Inhibitors
Symptomology
Development Summary
Site of Action Summary
Injury Symptoms
Time-lapsed Video 1
Time-lapsed Video 2
Herbicide
Families
Herbicides
Symptomology Development Summary
These herbicides inhibit lipid biosynthesis and are commonly referred to as “the –fops and –dims,” due to the similar endings of herbicide names (i.e. fluazifop,diclofop, clethodim, sethoxydim, etc.). Lipids are the building blocks of cell membranes. Lipid biosynthesis occurs mostly at the meristems of the root and shoot where new cells are being formed. Loss of lipid biosynthesis prohibits new cell membrane formation and thus new cell formation. The enzyme of action in grasses is sensitive while the enzyme site for this reaction in broadleaves is not sensitive.
Symptoms include discoloration
and disintegration of grass meristematic tissues, resulting in the rapid cessation
of root and shoot growth. The nodes become mushy and brown, the leaves turn
red or purple and yellow, and then wilt. The coloration changes are
largely due to the buildup of sugars in plant tissues caused by impeded translocation
system. Necrotic symptoms gradually spread over the entire plant often requiring
a week or more for complete plant death. Seedling grasses tend to lodge by
breaking at the soil line. At sub-lethal doses flowering and seed head production
of perennial grasses may be inhibited.
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These herbicides inhibit
the enzyme carboxyltransferase
an ACCase (Acetyl-CoAesterase), which speeds the formation of malonyl-CoA
from acetyl-CoA and CO2. Malonyl-CoA and acetyl-CoA are the building
blocks of phospholipids and triacylglycerols. Phospholipids and triacylglycerols
combine to form lipid bilayers that serve as the cellular membranes. Affected
plants cannot produce new cell membranes. This takes place in the grass’s
meristematic tissue, which explains the mushy and disintegrated growing point.
Disintegrated growing points can be easily separated from the plants due to
lack of membrane production.
Selectivity is based on proteins produced in monocots (grasses) versus dicots
(broadleaves). Monocots and dicots both possess ACCase enzymes in their cytoplasm
and chloroplasts. Dicots have a prokaryotic form of the enzyme in the chloroplast
and the eukaryotic form in the cytoplasm. Monocots have the eukaryotic form
in both their cytoplasm and chloroplasts. Only production of the eukaryotic
form is inhibited.
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Symptoms include discoloration
and disintegration of grass meristematic tissues, resulting in the cessation
of shoot growth. The leaf sheaths at the nodes become mushy and brown, and
the leaves themselves turn yellow and wilt. Necrotic symptoms gradually spread
over the entire plant; a week or more is required for complete plant death.
Seedling grasses tend to lodge by breaking over at the soil line. At sublethal
doses flowering and seedhead production of perennial grasses may be inhibited.
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