Suppose a person is homozygous for a mutation in the IRP gene that causes the IR

Question

Suppose a person is homozygous for a mutation in the IRP gene that causes the IRP protein to not bind iron, but can still bind to the IRE element.

How would this mutation affect the regulation of the transferrin receptor mRNA?

IRP would not bind to the mRNA even when iron is high, and translation of the mRNA is stopped when iron is high.

IRP remains bound to the mRNA even when iron is high, and translation of the mRNA is stopped when iron is high.

IRP would not bind to the mRNA even when iron is high, and translation of the mRNA is continued even when iron is high.

IRP remains bound to the mRNA even when iron is high, and translation of the mRNA is continued even when iron is high.

IRP would not bind to the mRNA even when iron is high, and translation of the mRNA is stopped when iron is high.

IRP remains bound to the mRNA even when iron is high, and translation of the mRNA is stopped when iron is high.

IRP would not bind to the mRNA even when iron is high, and translation of the mRNA is continued even when iron is high.

IRP remains bound to the mRNA even when iron is high, and translation of the mRNA is continued even when iron is high.

Explanation / Answer

This person would be unable to make ferritin, because the IRP would always be bound to the IRE. The amount of transferrin receptor mRNA would be high,even in the presence of high amounts of iron, because the IRP would always remain bound to the IRE and stabilize the transferrin receptor mRNA. This person would take up a lot of iron via the transferrin receptor, even when the iron concentrations were high. When iron levels are high, the person would continue to synthesize the transferrin receptor, which functions in the uptake of iron.

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