Photosystem II inhibitors are a common type of herbicide used for the control of many broadleaved weeds as well as some grasses. Most of these herbicides function by blocking the electron transport chain, something that's often achieved through binding of the herbicide to the D1 reaction center proteins of the secondary quinone acceptor site. This inhibits the reduction of plastoquinone. Explain why this would make it impossible for the plant to synthesize sugar molecules from G3P. Please include details on all relevant steps of the light-dependent reactions in your answer.
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Bonus: A herbicide blocks the light reaction of photosynthesis. Therefore, what is being blocked by this herbicide and killing the plant? (What does the light reaction do?) The herbicide prevents chlorophyll from being converted to protein. The herbicide prevents chlorophyll from being converted to sugar for carbohydrate production. The herbicide prevents light energy from being converted into chemical energy for the dark cycle. The herbicide prevents CO2 from being used in respiration.
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You are an intern at a company developing herbicides to use against invasive plant species. The team has already collected some data about the effects of these herbicides. Your job is to determine the mechanism of action for each herbicide (the way it affects the chloroplast to block photosynthesis). Why would blocking photosynthesis be a good way to kill plants? The first set of data describes NADPH production (ng/mol) before and 10 minutes after herbicide addition. When in photosynthesis is NADPH normally produced? What is it used for?
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