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Fig. 3 | Genome Biology

Fig. 3

From: Lifestyle modifications: coordinating the tRNA epitranscriptome with codon bias to adapt translation during stress responses

Fig. 3

Patterns of synonymous codon usage define families of stress-response genes and might predict epitranscriptomic responses to viral infections. a The idea that translation regulation uses auxiliary genetic information in the form of codon bias arose by linking systems-level analyses of stress-induced proteomic upregulation and downregulation [21, 28, 34] with codon analytics [28, 38]. The heat maps shown here are examples of genome-level application of a codon-counting algorithm and visualization approaches [28, 34] to the genomes of Mycobacterium bovis BCG and Saccharomyces cerevisiae. The maps show over-use (yellow) and under-use (purple) of 62 codons (columns) across all genes (rows). For each organism, clusters represent groups of genes that have distinctly different codon-usage patterns compared with genome averages, with two opposing groups of genes identified in humans. As shown in Fig. 2d, the smaller of two clusters of codon-biased genes in M. bovis BCG consists of the DosR regulon of 48 genes that control the response to hypoxic stress [34]. b Widely differing codon-usage patterns in the human genome and a representative dengue serotype 2 genome (DENV2) could predict reprogramming of the host cell tRNA epitranscriptome both to accommodate the codon mismatch in the viral RNA genome and to respond to the stress of viral infection. Codon frequency data were generated using the web-analysis interface on the published Codon Utilization Tool (CUT) [56] and the publicly available human and dengue sequence information (Human refseq_hg38 and dengue virus 2, complete genome NCBI Reference Sequence: KM204118.1), together with human and dengue frequency data found in Additional file 1. The analysis shows that the DENV2 genome is biased toward A-ending codons, whereas the human genome is biased toward G- and C-ending codons. This leads to the testable hypothesis that DENV2 infections will cause changes in the host cell tRNA pool, both modifications and copy numbers, to simultaneously accommodate translation of the viral mRNA and facilitate translation of codon-biased host stress-response genes

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