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EIF1-eIF4G1 inhibitors uncover alternative translation activation of stress-response genes via enhanced ribosome loading and 5’UTR translation [Ribo-Seq and Ti-Seq]

ABSTRACT: eIF1-eIF4G1 inhibitors uncover alternative translation activation of stress-response genes via enhanced ribosome loading and 5’UTR translation [Ribo-Seq and Ti-Seq]

PROVIDER: PRJNA701894 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR13711200.fastq.gz	Fastqsanger.gz
	SRR13711201.fastq.gz	Fastqsanger.gz
	SRR13711202.fastq.gz	Fastqsanger.gz
	SRR13711203.fastq.gz	Fastqsanger.gz
	SRR13711204.fastq.gz	Fastqsanger.gz

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eIF1-eIF4G1 inhibitors uncover alternative translation activation of stress-response genes via enhanced ribosome loading and 5’UTR translation [Ribo-Seq and Ti-Seq]

Project description:The Ribo-seq and TI-seq analysis following i14G1s (eI1-eIF4G1 inhibitors) treatments uncover opposing roles of eIF1-eIF4G1 and eIF4E-eIF4G1 in scanning-dependent and independent translation. Furthermore, i14G1s inhibition of eIF4G1-eIF1 resulted in translation activation of ER/UPR stress-response genes via enhanced ribosome loading, elevated 5’UTR translation at near cognate AUGs, and unexpected concomitant upregulation of coding-region translation.

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eIF1-eIF4G1 inhibitors uncover alternative translation activation of stress-response genes via enhanced ribosome loading and 5’UTR translation [MARS-seq]

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eIF1-eIF4G1 inhibitors uncover alternative translation activation of stress-response genes via enhanced ribosome loading and 5’UTR translation

Project description:eIF1-eIF4G1 inhibitors uncover alternative translation activation of stress-response genes via enhanced ribosome loading and 5’UTR translation

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Study of the eIFG1-eIF1 interaction by TCP-seq on translation initiation in HEK 293T cells

Project description:Start codon recognition by the 48S complex is a critical step in translation. However, understanding the in vivo initiation and its regulation at a global scale is limited. Here, we analyzed translation complex profiling (TCP-seq) data to determine the impact of eIF4G1-eIF1 inhibition and the 48S organization. Our analysis provides the first global view of leaky scanning and reveal the central roles of mRNA features and eIF4G1-eIF1 in its regulation. Specifically, non-leaky genes are enriched with a Kozak bearing a C at -1 position while those with short 5’ UTR with TISU. Additionally, the stability of the 48S complex and its integrity during scanning are impaired upon eIF4G1-eIF1 inhibition. Detailed analysis of initiation site footprints revealed three main classes conserved from yeast to human. Our analysis provides a general overview of AUG selection and evidence for conformational rearrangements in vivo.

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eIF1-eIF4G1 inhibitors uncover alternative translation activation of stress-response genes via enhanced ribosome loading and 5’UTR translation [MARS-seq]

Project description:eIF1-eIF4G1 inhibitors uncover alternative translation activation of stress-response genes via enhanced ribosome loading and 5’UTR translation [MARS-seq]

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Study of the translation initiation by Selective TCP-seq in the context of eIF1-eIF4G1 inhibitor

Project description:Start codon recognition by the 48S complex is a critical step in translation. However, understanding the in vivo initiation and its regulation at a global scale is limited. To better understand the mechanism in vivo, we have screened for small molecules that specifically inhibit the function of eIF1-eIF4G1 interaction. We performed Selective-48S footprinting against eIF1 (HA-tagged), eIF2a (HA-tagged), eIF4G1 and eIF3c to answer questions regarding the function of that interaction in the context of the scanning and initiating 48S ribosome.

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eIF1 discriminates against suboptimal initiation sites to prevent excessive uORF translation genome-wide

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Project description:Regulated translation initiation has the potential to reshape the proteome, but conditions under which start codon selection is altered remain poorly defined. Here, using global translation initiation site profiling, we reveal widespread changes in start codon selection during the mammalian cell cycle. Low-efficiency initiation sites are preferentially repressed in mitosis, resulting in changes in the relative translation of thousands of annotated proteins, alternative translational isoforms, and uORFs. This increased mitotic translational stringency results from the cytoplasmic release of a nuclear pool of eIF1 upon nuclear envelope breakdown. Increased eIF1-40S ribosome interactions repress suboptimal initiation sites to rewire the mitotic proteome. Selectively depleting the nuclear pool of eIF1 eliminates changes to translational stringency during mitosis, resulting in substantially increased cell death following an extended mitotic delay induced by anti-mitotic chemotherapeutics. Thus, cells globally control translation initiation stringency to alter their physiology with critical roles during the mammalian cell cycle.

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eIF1 modulates the recognition of sub-optimal translation start sites and steers gene expression control mediated by uORFs

Project description:Alternative translation initiation mechanisms such as leaky scanning and reinitiation potentiate the polycistronic nature of transcripts. By allowing for reprogrammed translation, these mechanisms can mediate biological responses to stress stimuli. We combined proteomics with ribosome profiling and mRNA sequencing to identify the biological targets of translation control triggered by eukaryotic translation initiation factor 1 (eIF1), a protein implicated in the stringency of start codon selection. We quantified expression changes of over 4,000 proteins and 10,000 actively translated transcripts, leading to the identification of 245 transcripts undergoing translational control mediated by upstream open reading frames (uORFs) upon eIF1 deprivation. The stringency of start codon selection and preference for optimal nucleotide context were largely diminished leading to translational regulation of uORFs with sub-optimal start sites. Affected genes were implicated in energy production and sensing of metabolic stress. Interestingly, knockdown of eIF1 elicited a synergic response from eIF5 and eIF1B.

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