Lecture 14 - Group 4 Flashcards
mode of action for group 4
auxinic herbicides (impacts hormones/auxin inhibitors)
how is group 4 applied
foliar application
what does group 4 control
selective control of broadleaves in cereal crops
how does the group 4 mode of action work
it binds to auxin-binding proteins in cytosol or plasma membrane and act as a mimic of the IAA resulting in rapid growth (plants grow themselves to death
symptoms of group 4 in dicots
- epinasty (twisting or downwards curling of leaves/upper stem grows faster than lower)
- leaf cupping
- adventitious roots
- callus growth
- chlorosis and necrosis
- initial symptoms right after, 3-4 weeks until death
symptoms of group 4 in monocots
- rapid chlorosis of new leaves
- general chlorosis and necrosis
what are the injury symptoms when a group 4 is applied late to resistant cereal crops
- abnormal seed head emergence
- abnormal or missing spikelets
- abnormal brace root development
basis of selectivity of group 4
- difference in morphology (leaf angle in mono and dicots)
- translocation and metabolism of herbicides in dicots and monocots
- monocots are generally tolerant
why are monocots generally more tolerant to group 4 than dicots
- they dont have cambium layer (which is sensitive to crushing in dicots)
- have differential binding to auxin binding proteins
peculiarities of group 4
- common in mixes
- drift prone
- cannot be mixed with group 1
- variable persistence depending on chemical
examples of soil persistence in group 4
- 2,4-D MCPA for 4-6 wks in warm, moist soils
- clopyralids can affects peas and fababean the following year
- picloram affects sensitive plants like lentils and potatoes
- quinclorac has extensive re-crop restrictions
mode of action for group 5, 6, and 7
photosynthetic inhibitors (inhibit photosystem 2) that causes the rapid production of toxic radicals that are quickly damaging
differences between group 5, 6, and 7 mode of action
all affect the same protein but:
- 6 has a different binding site
- 5 has same binding site as group 7 but different binding behavior
group 5 herbicides
- uracils
- S-triazinediones
- triazines
- pyridazinone
how does group 5 mode of action work
- inhibit photosystem 2 (collects light and supplies electrons) by affecting the binding of plastoquinone to site A and causes high energy electrons to cause damage to membranes
symptoms of group 5
-develop rapidly, especially in bright light
- injury in older leaves and edges of leaves
- some bleaching injury but not contact injury
- necrosis and chlorosis
selectivity of group 5
- wide range of selectivity
- selectivity by rapid herbicide metabolism to non-toxic metabolites
- also could be due to increased cytochrome and glutathione-S-transferase
peculiearities in group 5
-resistance in many weed species
- resistant biotypes suffer fitness penalty (yield less)
- often soil applied
group 6 herbicides
nitriles (bromoxynil)
how does group 6 mode of action work
bind to site B to prevent plastoquinone availability to accept electrons and cause death through free radical accumulation
symptoms of group 6
- blotchy, inter-venial chlorotic patches in leaves (first appear in leaf margin)
- rapid necrosis in leaf tissue
selectivity of group 6
- metabolism differential related to increased cytochrome P450 metabolism
- damage if applied under stressful conditions
peculiarities of group 6
- BT canola
- very few resistant weeds (common groundsel and lambs quarters)
