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During most eukaryotic translation processes, the small 40S ribosome subunit scans an mRNA from its 5' end until it encounters the first start AUG codon. The large 60S ribosomal subunit then joins the smaller one to initiate protein synthesis. The location of the translation initiation is largely determined by the nucleotides near the start codon as there may be multiple translation initiation sites present on the mRNA.  Marilyn Kozak discovered that the sequence RCCAUGG (where R...
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Initiating translation is complex because it involves multiple molecules. Initiator tRNA, ribosomal subunits, and eukaryotic initiation factors (eIFs) are all required to assemble on the initiation codon of mRNA. This process consists of several steps that are mediated by different eIFs.
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Translation is the process of synthesizing proteins from the genetic information carried by messenger RNA (mRNA). Following transcription, it constitutes the final step in the expression of genes. This process is carried out by ribosomes, complexes of protein and specialized RNA molecules. Ribosomes, transfer RNA (tRNA), and other proteins produce a chain of amino acids—the polypeptide—as the end product of translation.
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Lesson: Translation
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Base complementarity between the three base pairs of mRNA codon and the tRNA anticodon is not a failsafe mechanism. Inaccuracies can range from a single mismatch to no correct base pairing at all. The free energy difference between the correct and nearly correct base pairs can be as small as 3 kcal/ mol. With complementarity being the only proofreading step, the estimated error frequency would be one wrong amino acid in every 100 amino acids incorporated. However, error frequencies observed in...
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Stop Codon Context-Specific Induction of Translational Readthrough.

Mirco Schilff1, Yelena Sargsyan1, Julia Hofhuis1,2

  • 1Department of Child and Adolescent Health, University Medical Center, 37075 Göttingen, Germany.

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|August 6, 2021
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Summary
This summary is machine-generated.

Stop codon context significantly impacts the effectiveness of drugs designed to treat genetic diseases caused by premature termination codons (PTCs). Tailoring drug choice and concentration to the specific stop codon context offers a personalized medicine approach for rare genetic disorders.

Keywords:
PEX5aminoglycosideperoxisomeperoxisome biogenesis disorderpersonalized medicinerare diseasereadthrough therapytranslational readthrough

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Area of Science:

  • Genetics
  • Molecular Biology
  • Pharmacology

Background:

  • Premature termination codon (PTC) mutations are responsible for about 10% of pathogenic variants in monogenic diseases.
  • Translational readthrough-inducing drugs (TRIDs) offer a therapeutic strategy for genetic diseases caused by PTCs by promoting stop codon suppression.
  • The stop codon context (SCC), including the stop codon and surrounding nucleotides, influences readthrough efficiency, but its quantitative impact is not well understood.

Purpose of the Study:

  • To analyze the readthrough-stimulatory effect of various TRIDs on different SCCs of five common PTC mutations in the PEX5 gene.
  • To investigate the influence of SCC on treatment outcomes and optimal drug concentrations for PTC diseases.

Main Methods:

  • Utilized a sensitive dual reporter system to assess drug-induced readthrough.
  • Tested multiple translational readthrough-inducing drugs (TRIDs) against various stop codon contexts (SCCs) associated with PEX5 mutations.
  • Quantified the levels of readthrough stimulation for each drug-SCC combination.

Main Results:

  • Demonstrated that the stop codon context (SCC) strongly influences the degree of readthrough stimulation achieved by TRIDs.
  • Showed that SCC impacts the selection of the most effective drug and its optimal concentration for therapeutic intervention.
  • Identified variations in drug efficacy based on the specific SCC of PEX5 mutations.

Conclusions:

  • The stop codon context is a critical factor in the efficacy of translational readthrough-inducing drugs.
  • An SCC-based strategy can enable personalized medicine approaches for treating rare genetic diseases caused by PTCs.
  • Understanding SCC is essential for optimizing TRID therapy and improving treatment outcomes for patients with genetic disorders.