According to Ainsworth (2005), approximately 2 to 5% of cystic fibrosis cases ar

Question

According to Ainsworth (2005), approximately 2 to 5% of cystic fibrosis cases are caused by a mutation that introduces a premature stop codon to the Cystic Fibrosis Transmembrane Conductance Regulator (CFTR) gene, ultimately translating a truncated and nonfunctional CFTR enzyme. Treatment of this type of cystic fibrosis might involve inducing the ribosome to read through premature stop codons. A drug called PTC124 interferes with the ribosome's ability to correctly read stop codons, inducing the ribosome to insert an amino acid instead of terminating translation. A CFTR enzyme with an altered amino acid is not ideal, but may have greater functionality than the truncated form. Therefore, human clinical trials of PTC124 were conducted Predict if nonsense-mediated mRNA decay (NMD) would be a problem for this treatment o Yes. PTC124 will also interfere with actual stop codons, resulting in stalled ribosomes that cannot detach from the mRNA molecule Yes. NMD prevents transcription of mRNA that contains a nonsense mutation, the ribosome never has a chance to read through the premature stop codon No. Exon-junction proteins that target mRNA for degradation are removed when the ribosome reads through the premature stop codon. No. NMD is a bacterial form of mRNA surveillance, whereas eukaryotes use nonstop mRNA decay and no-go decay to prevent synthesis of truncated proteins. No. NMD activates a series of enzymes that terminate translation, recycle stalled O ribosomes, and degrade abnormal mRNA C. Ainsworth. Nonsense mutations: running the red light. Nature 2005, 438:726-728

Explanation / Answer

Answer: Option E is correct.

Explanation:

NMD recognizes a stalled ribosome at the premature termination codon and activates RNA degrading enzymes. These enzymes cleave the abnormal transcript thereby eliminating the production of truncated proteins which would sometimes behave in a dominant negative manner.

In the given case, PTC124 enables ribosome to read through the premature stop codon. So, NMD cannot be activated.

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