Herbicides Flashcards

1
Q

Tilling negatives and positives?

A

Gets rid of weeds, fairly low labour

Can degrade soil quality in surface nutrients and produce more run off

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2
Q

What is the loss of profit due to weeds growing in Australia?

A

3.3 Billion dollars $ in expenditure and loss

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3
Q

Main types of pesticides and herbicides used?

A

Glyphosate (round up), atrazine, Acetochlor (all herbicides US)

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4
Q

Side effect of Sinox (earliest developed herbicide?) and method for this?

A

Respiratory uncoupler binds to H atoms in intermembrane space and passes straight through membrane. This means the gradient of electrons cannot build during respiration and no ATP can form

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5
Q

Issues faced with herbicides?

A

Minimise- resistance
mammalian toxicity
persistance in environment

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6
Q

How does atrazine function?

A

Binds with D1 protein and hence competes with plastoquinone which is a shuttle for electrons in photosystem 2. It normally is reduced by D1 then passes on electron but when this cannot occur, starvation and oxidative damage TO PLANTS ONLY

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7
Q

How come atrazine doesnt affect crops?

A

Only specifically affects broadleaf leaves

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8
Q

How is maize resistant to atrazine?

A

Contains soluble enzyme glutathione transferase that can detoxify the molecule of atrazine by binding to glutathione. no longer can affect photosystem 2.

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9
Q

What is another effect of atrazine?

A

Mimicks eostregon (endocrine disruptor) can have low birthrate effects and affect sex of animals. Long half life (up to 261 days) means it can have lasting effects.

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10
Q

How are weeds now resistant?

A

Mutation in psbA gene from SER->GLY changes D1 protein now meaning the affinity to atrazine is lowered.

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11
Q

How does glyphosate function?

A

Intefers with shikimate pathway that results in three major amino acids (tryp, tyr, phenol). Stops EPSP synthase adding EPSP to 3-phosphate-shikimate.

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12
Q

Why is this not dangerous for humans?

A

Since this pathway is not present in humans, it is not dangerous for us.

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13
Q

Where did scientists isolate the gene for glyphosate resistance from?

A

From bacteria (agrobacterium) in 1983. It has a different shaped EPSP enzyme that does not get inhibited by glyphosate.

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14
Q

Construct for soybean resistance to glyphosate

A

35s promotor Nos terminator cp4 EPSP gene Plastid targetting sequence to get into chloroplast (requires n terminal targetting sequence to guide to port to chloroplast)

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15
Q

What was the error spotted 6 years after release of round up resistance?

A

Cheeky inversion as a result of tDNA process.

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16
Q

What is the danger of glyphosate?

A

Not yet proven to be cancer causing but lawsuits exist against monsanto

17
Q

IAA stands for?

A

Indol acetic acid (auxin) growth hormone

18
Q

How is it used as a herbicide?

A

Doesn’t affect humans. Can spray and tell plants to grow uncontrollably.

19
Q

What had to be adjusted in IAA to make it a good herbicide?

A

Make it more stable.

20
Q

What was agent Orange and what was its purpose?

A

2,4 D Auxin analogue - to kill all trees in the Vietnam war. It had side effects resulting in dioxins that affected birth defects.

21
Q

What is put into crops to make it resistant to 2,4 D?

A

Enzyme AAD - discovered in soil bacteria - detoxifys 24D

22
Q

Describe construct for 2,4D resistance

A

Ubi10 (constant) promoter, aad gene from soil bacteria, selectable marker (pat).

23
Q

How can roundup and 2,4D be used together?

A

Make plants with double resistance that you can then alternate between herbicides and stop other crops.