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Activation of GCN2 by Ribosome Stalling Links Translation Elongation with Translation Initiation

ABSTRACT: Activation of GCN2 by Ribosome Stalling Links Translation Elongation with Translation Initiation

PROVIDER: PRJNA317428 | ENA |

REPOSITORIES: ENA

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Activation of GCN2 kinase by ribosome stalling links translation elongation with translation initiation.

Project description: Not available

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Activation of GCN2 by Ribosome Stalling Links Translation Elongation with Translation Initiation

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2016-06-15 | E-GEOD-79930 | biostudies-arrayexpress

Activation of GCN2 by Ribosome Stalling Links Translation Elongation with Translation Initiation

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

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Codon usage and protein length-dependent feedback from translation elongation to translation initiation and kinetics

Project description:In yeast and mammals, activated GCN2 can phosphorylate its substrate eIF2α, which is a part of the eIF2-GTP-Met-tRNAiMet ternary complex. The eIF2α phosphorylation blocks the ternary complex formation and therefore inhibits translation initiation. Meanwhile, GCN2 activation associates with ribosomes and some translation elongation factors such as eEF1A. In Neurospora crassa, the homolog of GCN2 is CPC-3. Ribosome profiling and accompanying RNA-seq experiments in this project were used to explore the effects of CPC-3 on translation kinetics. Here we show that poor codon usage of mRNAs with long CDS preferentially causes CPC-3 activation, which in turn suppresses the translation initiation and elongation in both codon usage and CDS length dependent manner.

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GCN2 suppresses TOP mRNA translation via LARP1

Project description:La-related protein 1 (LARP1) has been identified as a key translational inhibitor of terminal oligopyrimidine tract (TOP) mRNAs downstream of the nutrient sensing protein kinase complex, mTORC1. LARP1 exerts this inhibitory effect on TOP mRNA translation by binding to the mRNA cap and the adjacent 5’TOP motif, resulting in the displacement of the eIF4E complex from TOP mRNAs. In the present study, we identify a second nutrient sensing kinase GCN2 that converges on LARP1 to control TOP mRNA translation. GCN2 inhibits TOP mRNA translation via ATF4-dependent transcriptional induction of LARP1 mRNAs and GCN1-mediated recruitment of LARP1 to stalled ribosomes. We performed ATF4 ChIP-seq experiments in both WT and GCN2 KO MEFs with or without leucine deprivation.

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Examination of gene expression in cerebellum of mouse strains B6J, B6J-nmf205-/-, B6J-Gcn2-/- and B6J-nmf205-/-;Gcn2-/-.

Project description:Ribosome stalling during translation has recently been shown to cause neurodegeneration, yet the signaling pathways triggered by stalled elongation complexes are unknown. To investigate these pathways we analyzed the brain of B6J-nmf205-/- mice in which neuronal elongation complexes are stalled at AGA codons due to deficiencies in a tRNA Arg(UCU) tRNA and GTPBP2, a mammalian ribosome rescue factor. Increased levels of phosphorylation of eIF2Î± (Ser51) were detected prior to neurodegeneration in these mice and transcriptome analysis demonstrated activation of ATF4, a key transcription factor in the integrated stress response (ISR) pathway. Genetic experiments showed that this pathway was activated by the eIF2alpha kinase, GCN2, in an apparent deacylated tRNA-independent fashion. Further we found that the ISR attenuates neurodegeneration in B6J-nmf205-/- mice, underscoring the importance of cellular and stress context on the outcome of activation of this pathway. These results demonstrate the critical interplay between translation elongation and initiation in regulating neuron survival during cellular stress. Examination of gene expression in cerebellum and hippocampus for 4 mice strains derived from C57BL/6J (B6J) strain. Microarray data was performed for 3 week and 5 week old mice in both cerebellum and hippocampus for B6J and B6J-nmf205-/- three replicates each. RNA-Seq data was perform on cerebellum of mice 3 weeks old, three replicates for each genotype: B6J, B6J-nmf205-/-, B6J-Gcn2-/- and B6J-nmf205-/-;Gcn2-/-.

2016-06-15 | E-GEOD-79929 | biostudies-arrayexpress

Ethylene modulates the dynamics of translation via GCN2 and EIN2 in Arabidopsis under submergence

Project description:General translational repression is predicted as a key process to reduce energy consumption under hypoxia. We have previously showed that mRNA loading onto polysome is reduced in Arabidopsis under submergence. Here, we showed that plant stress activated GCN2 (general control nonderepressible 2) can phosphorylate eIF2a (Eukaryotic Initiation Factor 2a) in Arabidopsis under submergence, and this process is reversible after desubmergence. Compared to the wild-type, the reduction in polysome loading during submergence was less severe in the gcn2 mutant. Transgenic lines overexpressing GCN2 had more ATP and conferred better tolerance under submergence, suggesting that GCN2 might modulate the dynamics of translation to adjust the energy homeostasis under hypoxia. Interestingly, GCN2-eIF2a signaling was activated by ethylene under submergence. However, GCN2 activity was not affected in ein2-5 and eil1ein3 under submergence, suggesting that GCN2 activity was regulated by noncanonical ethylene signaling. In addition, the polysome loading was retained in both ein2-5 and etr1-1 under submergence, implying that ethylene modulated the dynamic translation under submergence via EIN2 and GCN2. Notably, our NGS analysis also demonstrated that EIN2 and GCN2 regulated the translation of 23 core hypoxia genes as well as 53% translational repressed genes under submergence. On the other hand, EIN2 and GCN2 also affected the expression of genes involved in hypoxic response, ethylene response, biotic stress and negative regulation of cytokinin signaling. Taken together, these demonstrated that entrapped ethylene triggers GCN2 and EIN2 to ensure the translation of stress required proteins under submergence and also provide a step stone for future investigation how eukaryotic cells modulate the translation to response for the changeable environments.

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Translation elongation factor 4 (LepA) contributes to tetracycline susceptibility by stalling elongating ribosomes

Project description:Translation elongation factor 4 (LepA) contributes to tetracycline susceptibility by stalling elongating ribosomes

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Selective stalling of human translation through small molecule engagement of the ribosome nascent chain

Project description:We use ribosome profiling to demonstrate the selectivity of a small molecule, PF-06446846 that inhibits translation of its target by selectively inducing ribosome-stalling in a nascent chain sequence dependent manner.

2017-06-05 | GSE94454 | GEO

Response to herbicide treatment in wild type and gcn2 at the transcription and translation level in Arabidopsis thaliana

Project description:To understand the role of GCN2 in stress response, the total transcript and translation state were compared between Arabidopsis thaliana wild type (ecotype Landsberg erecta) and gcn2 (Genetrap line GT8359, Cold Spring Harbor Laboratory) seedlings with or without herbicide chlorosufuron treatment RNA was fractionated using sucrose gradients into polysomal and nonpolysomal RNAs. We also determined overall total transcript levels. We used Affymetrix ATH1 microarrays.

2015-12-01 | GSE52117 | GEO

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