Codon-Driven Translational Efficiency Is Stable across Diverse Mammalian Cell States
Whether codon usage fine-tunes mRNA translation in mammals remains controversial, with recent papers suggesting that production of proteins in specific Gene Ontological (GO) pathways can be regulated by actively modifying the codon and anticodon pools in different cellular conditions. In this work,...
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| Autores principales: | , , , , , , |
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| Lenguaje: | inglés |
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PLOS
2019
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| Acceso en línea: | https://demo7.dspace.org/handle/123456789/452 |
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| _version_ | 1860822453134032896 |
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| author | Rudolph, Konrad Schmitt, Bianca M Villar, Diego White, Robert J Marioni, John Kutter, Claudia Odom, Duncan |
| author2 | Functional Morphology (FUNMORPH) |
| author_browse | Functional Morphology (FUNMORPH) Kutter, Claudia Marioni, John Odom, Duncan Rudolph, Konrad Schmitt, Bianca M Villar, Diego White, Robert J |
| author_facet | Functional Morphology (FUNMORPH) Rudolph, Konrad Schmitt, Bianca M Villar, Diego White, Robert J Marioni, John Kutter, Claudia Odom, Duncan |
| author_sort | Rudolph, Konrad |
| collection | DSpace |
| description | Whether codon usage fine-tunes mRNA translation in mammals remains controversial, with recent papers suggesting that production of proteins in specific Gene Ontological (GO) pathways can be regulated by actively modifying the codon and anticodon pools in different cellular conditions. In this work, we compared the sequence content of genes in specific GO categories with the exonic genome background. Although a substantial fraction of variability in codon usage could be explained by random sampling, almost half of GO sets showed more variability in codon usage than expected by chance. Nevertheless, by quantifying translational efficiency in healthy and cancerous tissues in human and mouse, we demonstrated that a given tRNA pool can equally well translate many different sets of mRNAs, irrespective of their cell-type specificity. This disconnect between variations in codon usage and the stability of translational efficiency is best explained by differences in GC content between gene sets. GC variation across the mammalian genome is most likely a result of the interplay between genome repair and gene duplication mechanisms, rather than selective pressures caused by codon-driven translational rates. Consequently, codon usage differences in mammalian transcriptomes are most easily explained by well-understood mutational biases acting on the underlying genome. |
| id | oai:localhost:123456789-452 |
| institution | DSPACE.FCHPT |
| language | English |
| publishDate | 2019 |
| publishDateRange | 2019 |
| publishDateSort | 2019 |
| publisher | PLOS |
| publisherStr | PLOS |
| record_format | dspace |
| spelling | oai:localhost:123456789-4522021-04-07T16:30:12Z Codon-Driven Translational Efficiency Is Stable across Diverse Mammalian Cell States Rudolph, Konrad Schmitt, Bianca M Villar, Diego White, Robert J Marioni, John Kutter, Claudia Odom, Duncan Functional Morphology (FUNMORPH) Evolutionary Ecology Group (EVECO) Ecosystem Management (ECOBE) Whether codon usage fine-tunes mRNA translation in mammals remains controversial, with recent papers suggesting that production of proteins in specific Gene Ontological (GO) pathways can be regulated by actively modifying the codon and anticodon pools in different cellular conditions. In this work, we compared the sequence content of genes in specific GO categories with the exonic genome background. Although a substantial fraction of variability in codon usage could be explained by random sampling, almost half of GO sets showed more variability in codon usage than expected by chance. Nevertheless, by quantifying translational efficiency in healthy and cancerous tissues in human and mouse, we demonstrated that a given tRNA pool can equally well translate many different sets of mRNAs, irrespective of their cell-type specificity. This disconnect between variations in codon usage and the stability of translational efficiency is best explained by differences in GC content between gene sets. GC variation across the mammalian genome is most likely a result of the interplay between genome repair and gene duplication mechanisms, rather than selective pressures caused by codon-driven translational rates. Consequently, codon usage differences in mammalian transcriptomes are most easily explained by well-understood mutational biases acting on the underlying genome. 2019-04-26T08:57:07Z 2019-04-26T08:57:07Z 11/05/16 https://demo7.dspace.org/handle/123456789/452 en PLOS |
| spellingShingle | Rudolph, Konrad Schmitt, Bianca M Villar, Diego White, Robert J Marioni, John Kutter, Claudia Odom, Duncan Codon-Driven Translational Efficiency Is Stable across Diverse Mammalian Cell States |
| title | Codon-Driven Translational Efficiency Is Stable across Diverse Mammalian Cell States |
| title_full | Codon-Driven Translational Efficiency Is Stable across Diverse Mammalian Cell States |
| title_fullStr | Codon-Driven Translational Efficiency Is Stable across Diverse Mammalian Cell States |
| title_full_unstemmed | Codon-Driven Translational Efficiency Is Stable across Diverse Mammalian Cell States |
| title_short | Codon-Driven Translational Efficiency Is Stable across Diverse Mammalian Cell States |
| title_sort | codon driven translational efficiency is stable across diverse mammalian cell states |
| url | https://demo7.dspace.org/handle/123456789/452 |
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