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      Sequences Promoting Recoding Are Singular Genomic Elements

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          Abstract

          The distribution of sequences which induce non-standard decoding, especially of shift-prone sequences, is very unusual. On one hand, since they can disrupt standard genetic readout, they are avoided within the coding regions of most genes. On the other hand, they play important regulatory roles for the expression of those genes where they do occur. As a result, they are preserved among homologs and exhibit deep phylogenetic conservation. The combination of these two constraints results in a characteristic distribution of recoding sequences across genomes: they are highly conserved at specific locations while they are very rare in other locations. We term such sequences singular genomic elements to signify their rare occurrence and biological importance.

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          Most cited references65

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          The nonsense-mediated decay RNA surveillance pathway.

          Nonsense-mediated mRNA decay (NMD) is a quality-control mechanism that selectively degrades mRNAs harboring premature termination (nonsense) codons. If translated, these mRNAs can produce truncated proteins with dominant-negative or deleterious gain-of-function activities. In this review, we describe the molecular mechanism of NMD. We first cover conserved factors known to be involved in NMD in all eukaryotes. We then describe a unique protein complex that is deposited on mammalian mRNAs during splicing, which defines a stop codon as premature. Interaction between this exon-junction complex (EJC) and NMD factors assembled at the upstream stop codon triggers a series of steps that ultimately lead to mRNA decay. We discuss whether these proofreading events preferentially occur during a "pioneer" round of translation in higher and lower eukaryotes, their cellular location, and whether they can use alternative EJC factors or act independent of the EJC.
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            Correlation between the abundance of Escherichia coli transfer RNAs and the occurrence of the respective codons in its protein genes.

            T Ikemura (1981)
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              Synonymous codon usage in Escherichia coli: selection for translational accuracy.

              In many organisms, selection acts on synonymous codons to improve translation. However, the precise basis of this selection remains unclear in the majority of species. Selection could be acting to maximize the speed of elongation, to minimize the costs of proofreading, or to maximize the accuracy of translation. Using several data sets, we find evidence that codon use in Escherichia coli is biased to reduce the costs of both missense and nonsense translational errors. Highly conserved sites and genes have higher codon bias than less conserved ones, and codon bias is positively correlated to gene length and production costs, both indicating selection against missense errors. Additionally, codon bias increases along the length of genes, indicating selection against nonsense errors. Doublet mutations or replacement substitutions do not explain our observations. The correlations remain when we control for expression level and for conflicting selection pressures at the start and end of genes. Considering each amino acid by itself confirms our results. We conclude that selection on synonymous codon use in E. coli is largely due to selection for translational accuracy, to reduce the costs of both missense and nonsense errors.
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                Author and article information

                Contributors
                +1801581-5207 , +1801585-2465 , john.atkins@genetics.utah.edu
                +1801581-7236 , ray.gesteland@genetics.utah.edu
                brave.oval.pan@gmail.com
                Journal
                978-0-387-89382-2
                10.1007/978-0-387-89382-2
                Recoding: Expansion of Decoding Rules Enriches Gene Expression
                Recoding: Expansion of Decoding Rules Enriches Gene Expression
                978-0-387-89381-5
                978-0-387-89382-2
                21 July 2009
                2010
                : 24
                : 301-320
                Affiliations
                [ID1 ]GRID grid.223827.e, ISNI 0000000121930096, Molecular Biology Program, , University of Utah, ; N. 2030 E. 15, Salt Late City, 84112-5330 U.S.A.
                [ID2 ]GRID grid.223827.e, ISNI 0000000121930096, Dept. Bioengineering, , University of Utah, ; Salt Lake City, 84112 U.S.A.
                [1 ]GRID grid.7872.a, ISNI 0000000123318773, Biochemistry Department, , University College Cork, ; Cork, Ireland
                [2 ]GRID grid.7872.a, ISNI 0000000123318773, Cork Cancer Research Centre, , University College Cork, ; Cork, Ireland
                Article
                14
                10.1007/978-0-387-89382-2_14
                7122551
                c551b79f-82a5-4144-b4da-a2b4f101ad9b
                © Springer Science+Business Media, LLC 2010

                This article is made available via the PMC Open Access Subset for unrestricted research re-use and secondary analysis in any form or by any means with acknowledgement of the original source. These permissions are granted for the duration of the World Health Organization (WHO) declaration of COVID-19 as a global pandemic.

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                © Springer-Verlag New York 2010

                stop codon,codon bias,codon usage bias,singular element,codon reassignment

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