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Differential expression analysis connects knock-downs of eIF3e and eIF3d with the MAP kinase signaling pathway

ABSTRACT: Differential expression analysis connects knock-downs of eIF3e and eIF3d with the MAP kinase signaling pathway

PROVIDER: PRJNA896488 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR22122961.fastq.gz	Fastqsanger.gz
	SRR22122962.fastq.gz	Fastqsanger.gz
	SRR22122963.fastq.gz	Fastqsanger.gz
	SRR22122964.fastq.gz	Fastqsanger.gz
	SRR22122965.fastq.gz	Fastqsanger.gz

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Differential expression analysis connects knock-downs of eIF3e and eIF3d with the MAP kinase signaling pathway

Project description:A prominent hallmark of cancer is deregulated protein synthesis. It is well established that various translation initiation factors (eIFs) are either overexpressed or under-expressed in numerous types of cancer. Recent studies suggest that rather than representing an indirect consequence of neoplasia, imbalanced expression of eIFs significantly contributes to cellular transformation, tumor development, cancer cell survival, metastasis and tumor angiogenesis. Among them, eIF3 stands out as the largest complex composed of 12 subunits with a modular assembly, where aberrant expression of one subunit leads to partially functional subcomplexes. Here we took advantage of well-established knockdowns of subunits d, e and h of human eIF3, all implicated in cancer, and investigated their impact on differential gene expression translatome-wide by Ribo-Seq. We demonstrate that eIF3e and eIF3d knock-downs result in reduced translation efficiency of numerous components of the MAPK signaling pathway, a pathway often upregulated in cancer, and pathways preventing genotoxic stress. Concurrently, depletion of eIF3d increased translation of proteins associated with membrane organelles, whereas eIF3e depletion increased expression of numerous ribosomal proteins, implicating eIF3e in controlling the balanced production of mature ribosomes. Overall, our data illustrate that individual eIF3 subunits exert specific translational control over a broad range of cellular transcripts.

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eIF3d controls the persistent integrated stress response

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eIF4E-independent translation is largely eIF3d-dependent

Project description:We study here how mRNAs are translated in an eIF4E1-independent manner by blocking eIF4E1 using a constitutively active version of eIF4E-binding protein (4E-BP). Via ribosome profiling we identify a subset of mRNAs that are still efficiently translated when eIF4E1 is inactive. We find that these mRNAs preferentially release eIF4E1 when eIF4E1 is inactive and bind instead to eIF3D via its cap-binding pocket. eIF3D then enables these mRNAs to be efficiently translated due to its cap-binding activity.

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eIF4E-independent translation is largely eIF3d-dependent

Project description:eIF4E-independent translation is largely eIF3d-dependent

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