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54 Cards in this Set

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What 2 ways do electrons have to get into the chloroplast for photosynthesis?
1) splitting of water
2) through PQ
What are the end products of the light reaction?
NADPH2, ATP, O2
What is cyclic electron flow?
when electrons move from Fxd to PQ and continue the light reaction
Do photosynthetic inhitiors shut down cyclic electron flow initially and why?
No because the herbicide shuts down the QB plastoquinonoe binding site but electrons already in the system can move cyclicly from Fxd to PQ
What is the mechanism of photosynthetic inhibitors?
bind to the QB plastoquinone binding site of the D1 protein in photosystem II
What are the effects that follow photosynthetic inhibition?
1) Blockage of electron flow inhibits the fromation of ATP and NADPH2 which suts down CO2 fixation
2) Forms radical molecules in response to the excess energy buildup
How can you measure photosynthetic stress?
through chlorophyll fluorescence
How are photosynthetic inhibitor herbicides absorbed?
root uptake and translocated via xylem
What are the classes of photosynthetic inhibitors?
triazines, substituted ureas, uracils, carbamates, benzonitriles, bentazon, pyrazon, pyridate
What is the mechanism of triazines?
bind to the QB-binding niche of the D1 protein at amino acid 264 of photosystem II
What symptoms of injury are seen with photosynthetic inhibitors?
triazines - interveinal chlorosis with green leaf veins
sub. ureas - veinal chlorosis
What is the tolerance mechanism for triazines?
metabolism, most generally glutathione conjugation
Which of the photosynthetic inhibitors is persistant?
triazines, particularly atrazine
What characteristics are seen in plants resistant to triazines?
1) slower growth rate
2) lower photosynthetic efficiency
3) lethal mutation due to seletion pressure (fitness is less)
What is the mechanism of resistance to triazine herbicides?
glycine substitution of serine in the binding niche
What is a hypothesized mechanism of telerance for some triazines in cotton?
rapid turnover of the D1 protein
As a class, triazines are what type of compound (i.e. acid, base, hydrophilic, lipophilic)?
weak bases with low water solubility
What is the primary means of uptake for substituted ureas?
root uptake translocated via the xylem (apoplastic)
What is the mechanism of resistance to substituted ureas?
threonine substitution of serine
What is the tolerance mechanism of unaffected plants for substituted ureas?
metabolism into non-herbicidal intermediates and placement for fruit and nut crops
What is the tolerance mechanism of unaffected plants for uracils?
metabolism- oxidation and glucose conjugation
How persistant are uracils?
very - half-life is 5-6 months
How are carbamates taken into the plant?
contact only
What is the tolerance mechanism of unaffected plants for carbamates?
metabolism, primarily hydroxylation and conjugation to glucose or other sugars
What are the contact herbicides for photosynthetic inhibitors?
carbamates, benzonitriles, bentazon, pyridate
Which mode-of-action would be effective against seedling tissue?
growth inhibitors
What are the 3 types of growth inhibition?
1) cell division inhibitors
2) cell wall/plant inhibitors
3) protein, nucleic acid or lipid metabolism growth inhibitors
What is the mechanism of cell division inhibitors?
prevent and/or disrupt microtuble formation
Explain the function of microtubules.
Microtubules are made of tubulin which are free in cytoplasm. Tubulin polymerizes and dissoociates continuously. Microtubules function in the spindle apparatus of chromosome separation in mitosis and in cell plate formation and cytoskeleton of the cell.
What are the functions of tubulin?
1) make sure in right spot
2) help bind things
3) moves protein
Are most growth inhibitors applied PRE, PPI, or POST?
PRE
Often referred to as mitotic poisons, which herbicide families causes cell division inhibition?
carbamates, dinitroanilines, DCPA, Dithiopyr and thiazopyr
What is the mechanism for carbamates that cause growth inhibition?
affect cell division through abnormal microtubule arrangement
What herbicide would be considered non-mobile?
dinitroanilines
What is the mechanism for dinitroanilines?
inhibits cell division (mitosis) specifically binds to tubulin, preventing the polymerization of microtubules
What symptoms do dinitroanilines cause?
thickened, club-like roots that appear pruned
What is the the soil/environmental behavior of dinitroanilines?
stays in top 1-3 inch; possible carryover; microorganisms involved in breakdown
What is the mechanism of dithiopyr?
inhibits mitosis in late prometaphase by causing a loss of microtubules by binding to MAP which is a protein necessary to stabilize growing microtubules
What are the symptoms caused by dithiopyr?
roots appear club-shaped
What is the mechanism of benzonitriles?
inhibits cell plate formation in the development of cell walls, also been shown to inhibit cellulose biosynthesis, limiting cell division
What is the mechanism of isoxaben?
kills plants by inhibiting cell wall biosynthesis (specifically cellulose biosynthesis, inhibiting emergence)
What is a characteristics symptom of bensulide and ethofumesate?
'leaf sealing' of broadleaves and 'buggy-whipping' of grasses
What growth inhibitors are no longer registered?
TCA and Dalapon
What is a way that corn gluten meal can be more soluble?
by enzymatically hydrolyzing it
What is the name of a biologically active dipeptide in hydrolyzed corn?
Alaninyl-Alanine
What part of the plant does Ala-Ala mainly affect?
roots, minimal effect on shoot growth
What time of the year should corn gluten be applied?
early spring and late summer
What is a characteristic symptom of lipid/fatty acid inhibition?
'leaf sealing' of broadleaves and 'buggy-whipping' of grasses
What is the mechanism for Substituted Amides?
inhibit VLCFA production
Substituted Amides can be applied PRE or PPI, how do each affect weeds?
PRE at top 0.25'' has slightly better broadleaf control particularly larger seeds by causing poor growth and inc injury
PPI at 1-3'' has better grass control
How does metam sodium work?
it is a thiocarbamates and a fumigant that is rapidly converted to methylisothiocyanate (MIC) in the presence of soil water which is phytotoxic and interferes with plant enzymatic reactions
What weeds does aryl-oxy-phenoxys and cyclohexandiones affect?
it is a post-grass material
What is the mechanism for aryl-oxy-phenoxys?
binds to the enzyme acetyl-CoA carboxylase which converts acetyl-CoA to malonyl-CoA, initial step in fatty acid synthesis
What is the tolerance of aryl-oxy-phenoxys?
tolerant plants have a different structure of the target enzyme, not allowing binding (inactivation to occur, metabolism is also a tolerance mechanism