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Identifying Amino Acid Overproducers Using Rare-Codon-Rich Markers
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Stop Codon Usage as a Window into Genome Evolution: Mutation, Selection, Biased Gene Conversion and the TAG Paradox.

Alexander T Ho1, Laurence D Hurst1

  • 1Milner Centre for Evolution, University of Bath, Bath, United Kingdom.

Genome Biology and Evolution
|July 22, 2022
PubMed
Summary

Stop codon usage varies, with TGA and TAG showing differential patterns. G+C content influences TGA use, potentially via gene conversion, while TAG

Keywords:
genome evolutionmolecular evolutionstop codon read-throughstop codon usagetranslation terminationtranslational read-through

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Area of Science:

  • Genomics
  • Molecular Biology
  • Evolutionary Biology

Background:

  • Protein-coding genes utilize three stop codons: TAA, TGA, and TAG.
  • These stop codons exhibit unequal usage, similar to synonymous codons.
  • Differential usage of TGA and TAG, despite identical nucleotide content, offers insights into evolutionary forces.

Purpose of the Study:

  • To investigate the factors driving the differential usage of TGA and TAG stop codons.
  • To understand the relationship between genomic G+C content and stop codon usage.
  • To explain the 'TAG paradox,' where TAG usage is unresponsive to G+C pressure in some species.

Main Methods:

  • Comparative genomic analysis of stop codon usage across diverse species.
  • Analysis of stop codon usage in relation to genomic G+C content and isochores.
  • Evaluation of mutation bias, selection, and gene conversion models.

Main Results:

  • TGA usage increases with G+C content across genomes and within the human genome.
  • This TGA trend is not explained by mutation bias-drift equilibrium alone.
  • In mammals and birds, high TGA usage is linked to G+C-biased gene conversion (gBGC) and A+T→G+C repair bias.
  • TAG usage is largely unresponsive to G+C pressure in bacteria and archaea, termed the 'TAG paradox'.

Conclusions:

  • G+C pressure, particularly through gBGC, is a major driver of TGA usage trends, overriding mutation bias and selection for optimal stop codons (TAA).
  • The 'TAG paradox' remains unexplained by current models, suggesting potential unknown selective pressures or complexities in gBGC.
  • Resolving the TAG paradox could reveal novel selective mechanisms or intricate details of gene conversion processes.