The effects of codon bias and optimality on mRNA and protein regulation
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Cellular and Molecular Life Sciences
REVIEW
The effects of codon bias and optimality on mRNA and protein regulation Fabian Hia1 · Osamu Takeuchi1 Received: 8 June 2020 / Revised: 5 October 2020 / Accepted: 12 October 2020 © Springer Nature Switzerland AG 2020
Abstract The central dogma of molecular biology entails that genetic information is transferred from nucleic acid to proteins. Notwithstanding retro-transcribing genetic elements, DNA is transcribed to RNA which in turn is translated into proteins. Recent advancements have shown that each stage is regulated to control protein abundances for a variety of essential physiological processes. In this regard, mRNA regulation is essential in fine-tuning or calibrating protein abundances. In this review, we would like to discuss one of several mRNA-intrinsic features of mRNA regulation that has been gaining traction of recent—codon bias and optimality. Specifically, we address the effects of codon bias with regard to codon optimality in several biological processes centred on translation, such as mRNA stability and protein folding among others. Finally, we examine how different organisms or cell types, through this system, are able to coordinate physiological pathways to respond to a variety of stress or growth conditions. Keywords Codon optimality · Codon bias · mRNA regulation · Protein regulation
Introduction The degeneracy of the genetic code entails that 61 codons encode 20 different amino acids. With the exception of methionine and tryptophan, all amino acids are encoded by synonymous codons. One of the pioneering studies of synonymous codons was published in 1972, in a paper exhibiting a method to calculate codon frequencies in yeast and seven bacteria [1]. From the computations performed, Goel and colleagues arrived at a conclusion that synonymous codons were not fully equivalent and alluded that these differences in codon frequency were likely due to codons conferring different rates of translation and therefore, a “selection pressure to maintain certain ratios among the synonymous codons” [1]. These findings were further supplemented by analyses of part of the Escherichia coli (E. coli) chromosome which showed that the frequencies of synonymous codons were non-random in coding sequences [2]. This systematic bias in codon frequencies in organisms would come to be known as ‘codon (usage) bias’. In 1980, Grantham and colleagues * Osamu Takeuchi [email protected]‑u.ac.jp 1
Department of Medical Chemistry, Graduate School of Medicine, Kyoto University, Kyoto, Japan
proposed the Genome Hypothesis which states that synonymous codons are used at different frequencies by different genomes, and that the usage remains constant for all genes within each genome [3]. In other words, every organism utilizes its own system of synonymous codons. Because synonymous codons are decoded at different rates, codons can be briefly classified into two categories, optimal and non-optimal. Broadly speaking, optimal codons are decoded faster and more efficiently than the
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