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Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human[ChIP-seq]

ABSTRACT: Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human[ChIP-seq]

PROVIDER: PRJNA910965 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22677773.fastq.gz	Fastqsanger.gz
	SRR22677774.fastq.gz	Fastqsanger.gz
	SRR22677775.fastq.gz	Fastqsanger.gz

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Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human [RNA-seq]

Project description:Ribosomal frameshifting refers to the process that ribosomes slip into +1 or -1 reading frame, thus produce chimeric trans-frame proteins. In viruses and bacteria, programmed ribosomal frameshifting can produce essential trans-frame proteins for viral replication or regulation of other biological processes. In humans, however, functional trans-frame protein derived from ribosomal frameshifting is scarcely documented. Combining multiple assays, we show that short codon repeats could act as cis-acting elements that stimulate ribosomal frameshifting in humans, abbreviated as CRFS hereafter. Using proteomic analyses, we identified many putative CRFS events from 32 normal human tissues supported by trans-frame peptides positioned at codon repeats. Finally, we show a CRFS-derived trans-frame protein (HDAC1-FS) functions by antagonizing the activities of HDAC1, thus affecting cell migration and apoptosis. These data suggest a novel type of translational recoding associated with codon repeats, which may expand the coding capacity of mRNA and diversify the regulation in human.

2023-05-01 | GSE220677 | GEO

Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human[ChIP-seq]

Project description:Ribosomal frameshifting refers to the process that ribosomes slip into +1 or -1 reading frame, thus produce chimeric trans-frame proteins. In viruses and bacteria, programmed ribosomal frameshifting can produce essential trans-frame proteins for viral replication or regulation of other biological processes. In humans, however, functional trans-frame protein derived from ribosomal frameshifting is scarcely documented. Combining multiple assays, we show that short codon repeats could act as cis-acting elements that stimulate ribosomal frameshifting in humans, abbreviated as CRFS hereafter. Using proteomic analyses, we identified many putative CRFS events from 32 normal human tissues supported by trans-frame peptides positioned at codon repeats. Finally, we show a CRFS-derived trans-frame protein (HDAC1-FS) functions by antagonizing the activities of HDAC1, thus affecting cell migration and apoptosis. These data suggest a novel type of translational recoding associated with codon repeats,which may expand the coding capacity of mRNA and diversify the regulation in human.

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Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human.

Project description:Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human.

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Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human [RNA-seq]

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Start codon-associated ribosomal frameshifting mediates nutrient stress adaptation

Project description:Start codon-associated ribosomal frameshifting mediates nutrient stress adaptation

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Project description:A translating ribosome is typically thought to follow the reading frame defined by the selected start codon. Using super-resolution ribosome profiling, here we report pervasive out-of-frame translation from the start codon. Unlike programmable frameshifting during elongation, start codon-associated ribosome frameshifting (SCARF) stems from the slippage of the initiating ribosome. Using a massively paralleled reporter assay, we uncovered sequence elements acting as SCARF enhancers or repressors, implying that start codon recognition is coupled with reading frame fidelity. This finding explains thousands of mass spectrometry spectra unannotated from human proteome. Mechanistically, we find that the eukaryotic initiation factor 5B (eIF5B) maintains the reading frame fidelity during the transition from initiation to elongation. Intriguingly, amino acid starvation induces SCARF by proteasomal degradation of eIF5B. The stress-induced SCARF products provide a degradative source to mitigate amino acid scarcity during starvation. Our findings illustrate the beneficial effect of divergent translation in nutrient stress adaptation.

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Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human.

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Ribosomal frameshifting at normal codon repeats recodes functional chimeric proteins in human.

Project description:This SuperSeries is composed of the SubSeries listed below.

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