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Error compensation of tRNA misacylation by codon–anticodon mismatch prevents translational amino acid misinsertion

Paper ID Volume ID Publish Year Pages File Format Full-Text
15233 1394 2011 15 PDF Available
Title
Error compensation of tRNA misacylation by codon–anticodon mismatch prevents translational amino acid misinsertion
Abstract

Codon–anticodon mismatches and tRNA misloadings cause translational amino acid misinsertions, producing dysfunctional proteins. Here I explore the original hypothesis whether mismatches tend to compensate misacylation, so as to insert the amino acid coded by the codon. This error compensation is promoted by the fact that codon–anticodon mismatch stabilities increase with tRNA misacylation potentials (predicted by ‘tfam’) by non-cognate amino acids coded by the mismatched codons for most tRNAs examined. Error compensation is independent of preferential misacylation by non-cognate amino acids physico-chemically similar to cognate amino acids, a phenomenon that decreases misinsertion impacts. Error compensation correlates negatively with (a) codon/anticodon abundance (in human mitochondria and Escherichia coli); (b) developmental instability (estimated by fluctuating asymmetry in bilateral counts of subdigital lamellae, in each of two lizard genera, Anolis and Sceloporus); and (c) pathogenicity of human mitochondrial tRNA polymorphisms. Patterns described here suggest that tRNA misacylation is sometimes compensated by codon–anticodon mismatches. Hence translation inserts the amino acid coded by the mismatched codon, despite mismatch and misloading. Results suggest that this phenomenon is sufficiently important to affect whole organism phenotypes, as shown by correlations with pathologies and morphological estimates of developmental stability.

Graphical abstractFigure optionsDownload full-size imageDownload as PowerPoint slideHighlights► For a majority of tRNAs, non-cognate amino acids with the greatest probability of being misloaded, match the codons with the greatest probability of being mismatched by the tRNA's anticodon. ► This property of error compensation is more stronger for regular polymorphisms than pathogenic ones. ► It is stronger in lizards with low developmental instability. ► It is stronger for rarely used codons and anticodons.

Keywords
Alignment; Homology; tRNA synthetase; RNA duplex stability; Base pairings; Developmental stability; Wobble position; Post-transcriptional tRNA transformation
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Error compensation of tRNA misacylation by codon–anticodon mismatch prevents translational amino acid misinsertion
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Publisher
Database: Elsevier - ScienceDirect
Journal: Computational Biology and Chemistry - Volume 35, Issue 2, April 2011, Pages 81–95
Authors
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Subjects
Physical Sciences and Engineering Chemical Engineering Bioengineering
Get Full-Text Now
Don't Miss Today's Special Offer
Price was $35.95
You save - $31
Price after discount Only $4.95
100% Money Back Guarantee
Full-text PDF Download
Online Support
Any Questions? feel free to contact us