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A 2-month-old, breast-fed baby that was normal at birth begins to develop GI problems and cirrhosis of the liver. Molecular analysis indicates a normal amount of galactose-1-phosphate uridyl transferase mRNA, but no observable enzyme activity. Which of the following would be the best possible explanation for this?
A. Gene deletion B. Nonsense mutation C. Premature transcription termination sequence in the DNA D. Promoter mutation E. RNA splicing mutation |
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i think the and is nonsense mutation bcos of early stop codon. pls post the ans.
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I also think D
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Yeh i think ur rt. it could be D
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you got it wrong guys.The correct answer is B.
A nonsense mutation is a mutation in the DNA that leads to a premature stop codon when the mRNA is being translated into protein. The mRNA would be transcribed correctly, but when the protein was being translated, it would be stopped prematurely, leading to a truncated protein. A promoter mutation in the DNA, if it caused the gene in question to be less actively transcribed would result in a diminished amount of message |
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No prob.i m posting one right now
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if the translation is terminated quickly then how could it become galactose 1 phosphate uridyl transferase it would become a different protein with less no of amino acids no sam pls explain it in a more detailed way
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Quote:
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now i understood laith thanks
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