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EIF3d controls the persistent integrated stress response

ABSTRACT: eIF3d controls the persistent integrated stress response

PROVIDER: PRJNA989225 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR25076917_1.fastq.gz	Fastqsanger.gz
	SRR25076917_2.fastq.gz	Fastqsanger.gz
	SRR25076918_1.fastq.gz	Fastqsanger.gz
	SRR25076918_2.fastq.gz	Fastqsanger.gz
	SRR25076919_1.fastq.gz	Fastqsanger.gz

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eIF3d controls the persistent integrated stress response

Project description:All cells respond to intrinsic and extrinsic stresses by reducing global protein synthesis and activating select gene programs necessary for survival. Here, we show the fundamental integrated stress response (ISR) is driven by the non-canonical cap-binding protein eIF3d which acts as a master effector to control core stress response orchestrators, the translation factor eIF2ɑ and the transcription factor ATF4. We find that during persistent stress, eIF3d activates translation of the protein kinase GCN2, inducing eIF2ɑ phosphorylation and inhibiting global protein synthesis. In parallel, eIF3d upregulates the m6A demethylase enzyme ALKBH5 to drive 5′ UTR-specific demethylation of stress response genes, including ATF4. Ultimately, this cascade converges on ATF4 expression by increasing mRNA engagement of translation machinery and enhancing ribosome bypass of upstream open reading frames. Our results reveal that eIF3d acts as a critical life-or-death decision point during adaptation to chronic stress and uncover a synergistic signaling mechanism in which translational cascades dynamically complement transcriptional amplification to control essential cellular processes.

2023-09-11 | GSE236188 | GEO

A phosphorylation-regulated eIF3d translation switch mediates cellular adaptation to metabolic stress

Project description:Shutoff of global protein synthesis is a conserved response to cellular stresses. This general phenomenon is accompanied by induction of distinct gene programs tailored to each stress condition. Although the mechanisms that lead to general repression of protein synthesis are well characterized, how cells reprogram the translation machinery for selective gene expression remains poorly understood. Here we show that the noncanonical 5′ cap-binding protein eIF3d is specifically activated in response to metabolic stress, due to loss of CK2-mediated phosphorylation near the eIF3d cap-binding pocket. Activated eIF3d controls a gene program enriched in factors important for glucose homeostasis, including members of the mTOR pathway, and eIF3d-mediated translation adaptation is essential for cell survival during chronic glucose deprivation. Our findings reveal a new mechanism of translation reprogramming engaged in response to metabolic stress.

2020-11-16 | GSE158249 | GEO

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.

2024-08-07 | GSE243708 | GEO

Dynamic O-GlcNAcylation of eIF3a controls translation reinitiation during integrated stress response

Project description:Dynamic O-GlcNAcylation of eIF3a controls translation reinitiation during integrated stress response

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Regulation of HCMV replication by eIF3d

Project description:Regulation of HCMV replication by eIF3d

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Integrated stress response

Project description:Comparison of genes induced during activation of the Integrated Stress Response by tunicamycin or following AP20187 induced dimerization of a Fv2E-PERK chimera in wildtype cells and cells carrying mutations in key ISR signaling molecules. Keywords: other

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eIF4E-independent translation is largely eIF3d-dependent

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

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Mitochondrial integrated stress response controls lung epithelial cell fate.

Project description:Alveolar epithelial type 1 (AT1) cells are necessary to transfer oxygen and carbon dioxide between the blood and air. Alveolar epithelial type 2 (AT2) cells serve as a partially committed stem cell population, producing AT1 cells during postnatal alveolar development and repair after influenza A and SARS-CoV-2 pneumonia1-6. Little is known about the metabolic regulation of the fate of lung epithelial cells. Here we report that deleting the mitochondrial electron transport chain complex I subunit Ndufs2 in lung epithelial cells during mouse gestation led to death during postnatal alveolar development. Affected mice displayed hypertrophic cells with AT2 and AT1 cell features, known as transitional cells. Mammalian mitochondrial complex I, comprising 45 subunits, regenerates NAD+ and pumps protons. Conditional expression of yeast NADH dehydrogenase (NDI1) protein that regenerates NAD+ without proton pumping7,8 was sufficient to correct abnormal alveolar development and avert lethality. Single-cell RNA sequencing revealed enrichment of integrated stress response (ISR) genes in transitional cells. Administering an ISR inhibitor9,10 or NAD+ precursor reduced ISR gene signatures in epithelial cells and partially rescued lethality in the absence of mitochondrial complex I function. Notably, lung epithelial-specific loss of mitochondrial electron transport chain complex II subunit Sdhd, which maintains NAD+ regeneration, did not trigger high ISR activation or lethality. These findings highlight an unanticipated requirement for mitochondrial complex I-dependent NAD+ regeneration in directing cell fate during postnatal alveolar development by preventing pathological ISR induction.

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