Question

Mutations that introduce stop codons cause a number of geneticdiseases. For example, from 2% to 5% of the people who have cysticfibrosis possess a mutation that causes a premature stop codon inthe gene encoding the cystic fibrosis transmembrane conductanceregulator (CFTR). This premature stop codon produces a truncatedform of CFTR that is nonfunctional and results in the symptoms ofcystic fibrosis. One possible way to treat people with geneticdiseases caused by these types of mutations is to trick theribosome into reading through the stop codon, inserting an aminoacid into its place. Although the protein produced may have onealtered amino acid, it is more likely to be at least partlyfunctional than is the truncated protein produced when the ribosomestalls at the stop codon. Indeed, geneticists have conductedclinical trials on people with cystic fibrosis with the use of adrug called PTC124, which interferes with the ribosome's ability tocorrectly read stop codons (C. Ainsworth, 2005, Nature438:726–728). On the basis of what you know about the mechanism ofnonsense-mediated mRNA decay (NMD), would you expect NMD to be aproblem with this type of treatment?

	Yes, NMD would be a problem, as it requires ribosome torecognize a specific stop codon.
	Yes, NMD would be a problem because even although the ribosomewould read through the stop codon, premature degradation of themRNA would take place.
	None of the above is true.
	No, NMD would not be a problem because the ribosome would readthrough the mutated stop codon, removing exon-junction proteinsthat would normally signal premature degradation of mRNA.
	No, NMD would not be a problem because it only occurs inprokaryotes.