Ontology highlight
ABSTRACT:
PROVIDER: PRJNA474899 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR7270890_1.fastq.gz | Fastqsanger.gz | |||
| SRR7270890_2.fastq.gz | Fastqsanger.gz | |||
| SRR7270900_1.fastq.gz | Fastqsanger.gz | |||
| SRR7270900_2.fastq.gz | Fastqsanger.gz | |||
| SRR7270891_1.fastq.gz | Fastqsanger.gz |
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Project description:<p>Persistent infection of mosquito vectors is essential for the transmission of arboviruses, yet how these viruses produce sufficient progeny without compromising host cell fitness remains unclear. Arbovirus genomes exhibit suboptimal codon usage for both human and mosquito hosts, raising questions about how they achieve efficient translation in such distinct cellular environments. Using chikungunya virus (CHIKV) as a model, we conducted a temporal, genome-wide analysis of transcription, translation, and tRNA modifications in Aedes albopictus C6/36 cells. We found that, unlike in human cells, CHIKV infection does not manipulate the tRNA modification landscape in mosquitoes to overcome codon bias. Instead, viral persistence is marked by a progressive, virus-specific repression of CHIKV RNA translation, occurring alongside a recovery of host mRNA translation. This translational balance, established independently of the RNAi system, supports sustained viral production without major disruption to host gene expression. Our findings reveal a fine-tuned equilibrium in mosquito cells that allows the establishment of long-term CHIKV persistence through controlled viral protein synthesis.</p>
2026-02-12 | MTBLS12760 | MetaboLights
Project description:Recent evidence indicates that codon usage bias regulates gene expression. How viruses, such as the emerging mosquito-borne Chikungunya virus (CHIKV), express their genomes at high levels despite an enrichment in rare codons remains a puzzling question. Using ribosome footprinting, here we analysed translational changes that occur upon CHIKV infection at the ER and the cytosol. We show that CHIKV infection induces codon-specific reprogramming of the host translation machinery to favor the translation of viral RNA genomes over host mRNAs with an otherwise optimal codon usage. This reprogramming was mostly apparent at the ER, where CHIKV RNAs are efficiently translated. Mechanistically, it involves CHIKV-induced overexpression of KIAA1456, an enzyme that modifies the wobble U34 position in the anticodon of tRNAs, which we find is required for proper decoding of codons that are highly enriched in CHIKV RNAs. Our findings demonstrate an unprecedented interplay of viruses with the host tRNA epitranscriptome to adapt the host translation machinery to viral production.
2025-06-16 | MTBLS2443 | MetaboLights
Project description:Differences in codon frequency between genomes, genes, or positions along a gene, modulate transcription and translation efficiency, leading to phenotypic and functional differences. Integrative studies quantifying the phenotypic consequences of codon usage bias at different molecular and cellular levels in human cells are lacking. Here, we present a multiscale analysis of the effects of synonymous codon recoding during heterologous gene expression in human cells. Six synonymous versions of an antibiotic resistance gene were generated, fused to a fluorescent reporter, and independently expressed in HEK293 cells. Multiscale phenotype was analysed by means of: quantitative transcriptome and proteome assessment, as proxies for gene expression; cellular fluorescence, as a proxy for single-cell level expression; and real-time cell proliferation in absence or presence of antibiotic, as a proxy for the cell fitness. We show that differences in codon usage bias strongly impact the molecular and cellular phenotype: (i) they result in large differences in mRNA and in protein levels, as well in mRNA-to-protein ratio; (ii) they introduce unpredicted splicing events; (iii) they lead to reproducible phenotypic heterogeneity; and (iv) they lead to a trade-off between the benefit of antibiotic resistance and the burden of heterologous expression. In human cells in culture, codon usage bias modulates gene expression by modifying mRNA availability and suitability for translation, leading to differences in protein levels and eventually eliciting functional phenotypic changes.
2024-05-24 | PXD038324 | Pride
Project description:Synonymous codon usage regulates translation initiation
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Project description:Codon usage influences the local rate of translation elongation to regulate co-translational protein folding
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Project description:Usage of synonymous codons represents a characteristic pattern of preference in each organism. It has been inferred that such bias of codon usage has evolved as a result of adaptation for efficient synthesis of proteins. Here we examined synonymous codon usage in genes of the fission yeast Schizosaccharomyces pombe, and compared codon usage bias with expression levels of the gene. In this organism, synonymous codon usage bias was correlated with expression levels of the gene; the bias was most obvious in two-codon amino acids. A similar pattern of the codon usage bias was also observed in Saccharomyces cerevisiae, Arabidopsis thaliana, and Caenorhabditis elegans, but was not obvious in Oryza sativa, Drosophila melanogaster, Takifugu rubripes and Homo sapiens. As codons of the highly expressed genes have greater influence on translational efficiency than codons of genes expressed at lower levels, it is likely that codon usage in the S. pombe genome has been optimized by translational selection through evolution. Relative amounts of mRNA for each ORF were measured by DNA microarray using genomic DNA as a reference, and the copy number of mRNA was calculated using an estimate of the total mRNA number in the cell as 100,000 copies.
2010-06-20 | E-GEOD-13554 | biostudies-arrayexpress
Project description:We have previously shown that the yeast homolog of the RNA-binding vigilin proteins – Scp160p – is involved in enhancing translation efficiency in the context of codon usage. In the current study, we investigated the influence of Scp160p on the biology of polyQ reporters which differ in the codon usage of their polyQ regions. We observe that Scp160p facilitates aggregation of the polyQ reporters independent of codon usage. To explore if Scp160p might also facilitate the aggregation of endogenous polyQ-containing proteins in the yeast proteome, we combined filter trap binding and dimethyl labeling mass spectrometry to assess the aggregation state of the proteome in scp160Δ cells. Filter trap binding allows the isolation of protein aggregates which are SDS-resistant (a feature of polyQ aggregates) from wild-type and scp160Δ cells. Dimethyl labeling with nanoLC-MS/MS provided a quantitative comparison of the amount of aggregated proteins isolated by filter trap binding.
2018-07-03 | PXD008175 | Pride
Project description:In eukaryotic ribosomes, ~2% of RNA nucleotides undergo 2'-O-methylation, a conserved cellular mechanism thought to be critical for maintaining and regulating translation. Here, we use ribosome profiling, translation assays, proteomics, and high-resolution structural analyses to show that loss of native 2'-O-methylation in yeast ribosomes disproportionally affect the translation of ribosomal protein transcripts, driven by changes in codon usage and recognition of structured RNA. Translation reprograming by the hypomethylated ribosomes is supported by reduced thermostability and high-resolution evidence of altered ribosomal structures and conformations. Consistent with the roles of the affected proteins in sustaining cellular fitness, hypomethylated ribosomes under stress exhibit selective loss of downregulated proteins and misassembly associated with methylation loss. Our data provide structural and mechanistic insights into how 2'-O-methylation supports ribosome integrity and mediates cellular stress responses.
2026-02-20 | MSV000100922 | MassIVE
Project description:Codon usage optimization in pluripotent embryonic stem cells [RNA-seq]
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