Question

DCMU is marketed as an algicide and an herbicide. It works by blocking the binding site for plastoquinone on photosystem II. You can see this diagramed in Figure 5.

a. If DCMU blocks plastoquinone from binding to photosystem II then in what state (oxidized or reduced) will the chlorophyll a of photosystem II be stuck? Why? (2 points)

b. Based on your answer above, in what state would plastoquinone be stuck? Why? (2 points)

c. Considering where DCMU binds, would plants in nature exposed to DCMU be able to produce ATP and NADPH through the light reactions? Why or why not? (2 points)

d. If plants exposed to DCMU cannot produce ATP and NADPH through the light reactions, how would this affect the light-independent reactions? (4 points)

e. DCMU, as an herbicide, will eventually kill plants that are exposed to it. Why is this the case? In answering this, relate DCMU to photosynthesis and both DCMU and photosynthesis to cellular respiration. (4 points)

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Answer 1

a. If DCMU blocks plastoquinone from binding to photosystem II then in what state (oxidized or reduced) will the chlorophyll a of photosystem II be stuck? Why? (2 points)

The chlorophyll a of photosystem II i.e. P680 is a strong oxidizing agent which is positively charged. It attracts an electron from an Electron donor to regenerate the P680+. Here P680 receives an electron from the photolysis of water. Thus if DCMU blocks plastoquinone from binding to PSII then chlorophyll a (P680) is stuck in a reduced state.

b. Based on your answer above, in what state would plastoquinone be stuck? Why? (2 points)

Plastoquinone will be present in an Oxidized state since it has a lower reduction potential and doesn't receive any electron from chlorophyll a.

c. Considering where DCMU binds, would plants in nature exposed to DCMU be able to produce ATP and NADPH through the light reactions? Why or why not? (2 points)

Considering where DCMU binds, plants in nature exposed to DCMU will not be able to produce ATP and NADPH through non-cyclic electron flow since DCMU blocks electron flow to plastoquinone and also to subsequent Cytb6f complex. Cytb6f complex is responsible for pumping protons into the Thylakoid lumen and when electron flow is blocked it doesn't pump any protons and thus no ATP is produced. NADPH is not produced since the electron never reaches the PS I.

However DCMU doesn't affect the production of ATP through the cyclic electron follow path since it doesn't involve plastoquinone or PSII .

d. If plants exposed to DCMU cannot produce ATP and NADPH through the light reactions, how would this affect the light-independent reactions? (4 points)

If plants exposed to DCMU cannot produce ATP and NADPH through the light reactions, then there will be no Dark cycle . ATP and NADPH produced by light-dependent phase reactions are utilized to produce food such as the 3 carbon compounds and ultimately starch from the CO2. Thus the plant will not be able to synthesize the required food and eventually die.

e. DCMU, as an herbicide, will eventually kill plants that are exposed to it. Why is this the case? In answering this, relate DCMU to photosynthesis and both DCMU and photosynthesis to cellular respiration. (4 points)

DCMU as an herbicide kills plants exposed to it because it prevents the production of ATP and also starch, which is the main stored food utilized by plants for survival. DCMU abolishes photosynthetic oxygen production since it competes with plastoquinone for the Qb binding site of PSII and blocks electron flow. No production of ATP means cellular respiration comes to a halt. In addition, the sequestered CO2 is not converted to starch. Thus the plant dies.