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Mammalian proteome expansion by stop codon readthrough.

Lekha E Manjunath1, Anumeha Singh1, Saubhik Som1

  • 1Department of Biochemistry, Indian Institute of Science, Bengaluru, Karnataka, India.

Wiley Interdisciplinary Reviews. RNA
|May 16, 2022
PubMed
Summary

Stop codon readthrough (SCR) allows translation to continue past a stop signal, producing altered proteins. Understanding SCR mechanisms in mammals may lead to new therapies for genetic diseases caused by premature stop codons.

Keywords:
frequencymRNAreadthroughstop codontranslation

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Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • Stop codon readthrough (SCR) is a biological recoding process where translation machinery recognizes a stop codon as a sense codon, bypassing termination.
  • This phenomenon occurs across all domains of life, including mammals, and influences protein diversity.

Purpose of the Study:

  • To review recent advances in understanding mammalian stop codon readthrough (SCR).
  • To propose a mechanism for SCR induction involving transient molecular roadblocks.
  • To explore therapeutic applications of SCR for diseases linked to premature stop codons.

Main Methods:

  • Review of recent technological and computational advancements in SCR research.
  • Analysis of molecular events during SCR in various mammalian mRNAs.
  • Integration of existing knowledge to propose a novel mechanistic model.

Main Results:

  • Recent advances have significantly enhanced the understanding of SCR in mammalian systems.
  • A model proposing transient molecular roadblocks downstream of the stop codon as an SCR inducer is presented.
  • SCR events offer insights for developing therapeutic strategies against premature stop codon diseases.

Conclusions:

  • Mammalian SCR is a complex process influenced by various mRNA features and interacting molecules.
  • Transient molecular roadblocks offer a plausible mechanism for SCR induction.
  • Harnessing natural SCR mechanisms presents a promising avenue for treating genetic disorders caused by premature termination signals.