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The translational protein 4E-T regulates the balance between differentiation and establishment of postnatal neural stem cell pools

ABSTRACT: Microarrays were performed (N=3) on postnatal precursors grown as neurospheres to determine level of gene expression To determine the transcript targets of the translational regulator 4E-T and whether these targets are repressed, we performed RIPs (GSE224966) for these targets as well as Ribotag (GSE224853) in addition to the following microarray as control to determine gene expression in posntatal precursors and ensure the differences observed in Ribotag were not simply due to differences in gene expression levels

ORGANISM(S): Mus musculus

PROVIDER: GSE225351 | GEO | 2024/02/12

REPOSITORIES: GEO

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The P-body protein 4E-T regulates the balance between cell genesis and establishment of the postnatal neural stem cell pool by repressing mRNA translation [4ET_neurosphere]

Project description:To investigate the targets of 4E-T in postnatal V-SVZ precursors cultured as neurospheres We performed RNA immunoprecipitations (RIPseq) on neurosphere lysates with anti-4E-T or control anti-IgG antibodies, isolated and sequenced the resulting RNA

2024-02-08 | GSE224966 | GEO

The P-body protein 4E-T regulates the balance between cell genesis and establishment of the postnatal neural stem cell pool by repressing mRNA translation [Ribotag]

Project description:To investigate the translatome of postnatal precursors of the V-SVZ cultured as neurospheres, we employed RiboTag analysis We performed RiboTag analysis on precursors derived from NestinCreERT2;RPL22HA/HA animals using specific anti-Hemagluttinin antibodies versus non-specific IgG controls

2024-02-08 | GSE224853 | GEO

An eIF4E1/4E-T complex determines the genesis of neurons from precursors by translationally repressing a proneurogenic transcription program

Project description:Here, we have addressed the mechanisms that determine genesis of the correct numbers of neurons during development, focusing upon the embryonic cortex. We identify in neural precursors a repressive complex involving eIF4E1 and its binding partner 4E-T that coordinately represses translation of proteins that determine neurogenesis. This eIF4E1/4E-T complex is present in granules with the processing body proteins Lsm1 and Rck, and disruption of this complex causes premature and enhanced neurogenesis and neural precursor depletion. Analysis of the 4E-T complex shows that it is highly enriched in mRNAs encoding transcription factors and differentiation-related proteins. These include the proneurogenic bHLH mRNAs, which colocalize with 4E-T in granules, and whose protein products are aberrantly upregulated following knockdown of eIF4E, 4E-T, or processing body proteins. Thus, neural precursors are transcriptionally primed to generate neurons, but an eIF4E/4E-T complex sequesters and represses translation of proneurogenic proteins to determine appropriate neurogenesis. We obtained 3 biological replicates of IgG-bound RNA, 4E-T-bound RNA, and cooresponding total RNA input from mouse E12-13 cortices. RNA samples were analyzed on the Affymetrix Mouse Gene 2.0 ST Arrays.

2014-09-25 | E-GEOD-61729 | biostudies-arrayexpress

An eIF4E1/4E-T complex determines the genesis of neurons from precursors by translationally repressing a proneurogenic transcription program

2014-09-25 | GSE61729 | GEO

The P-body protein 4E-T regulates the balance between cell genesis and establishment of the postnatal neural stem cell pool by repressing mRNA translation [Cpeb4_neurosphere]

Project description:To investigate the targets of Cpeb4/Cpeb4-associated transcripts in postnatal V-SVZ precursors cultured as neurospheres We performed RNA immunoprecipitations (RIPseq) on neurospheres using anti-Cpeb4 or control anti-IgG antibodies, isolated and sequenced the resulting RNA

2024-02-08 | GSE224854 | GEO

Project description:Eukaryotic translation initiation factor 4E (eIF4E)–binding protein 1 (4E-BP1) inhibits cap-dependent translation in eukaryotes by competing with eIF4G for an interaction with eIF4E. Phos-phorylation at Ser-83 of 4E-BP1 occurs during mitosis through the activity of cyclin-dependent kinase 1 (CDK1)/cyclin B rather than through canonical mTOR kinase activity. Here, we investi-gated the interaction of eIF4E with 4E-BP1 or eIF4G during interphase and mitosis. We observed that 4E-BP1 and eIF4G bind eIF4E at similar levels during interphase and mitosis. The most highly phosphorylated mitotic 4E-BP1 isoform (δ) did not interact with eIF4E, whereas a distinct 4E-BP1 phospho-isoform, EB-γ—phosphorylated at Thr-70, Ser-83, and Ser-101—bound to eIF4E during mitosis. Two-dimensional gel electropho-retic analysis corroborated the identity of the phosphorylation marks on the eIF4E-bound 4E-BP1 isoforms and uncovered a population of phosphorylated 4E-BP1 molecules lacking Thr-37/Thr-46–priming phosphorylation. Moreover, proximity ligation assays for phospho–4E-BP1 and eIF4E revealed different in situ interactions during interphase and mitosis. The eIF4E:eIF4G interaction was not inhibited, but rather increased in mitotic cells, consistent with active translation initiation during mitosis. Phospho-defective substitution of 4E-BP1 at Ser-83 did not change global translation or individual mRNA translation profiles as measured by single-cell nascent protein synthesis and eIF4G RNA-immunoprecipitation sequencing. Mitotic 5’-terminal oligopyrimidine RNA translation was active and, unlike interphase translation, resistant to mTOR inhibition. Our findings reveal the phosphorylation profiles of 4E-BP1 isoforms and their interactions with eIF4E throughout the cell cycle and indicate that 4E-BP1 does not specifically inhibit translation initiation during mitosis.

2019-06-14 | GSE131668 | GEO

4E-BP1 counteracts human stem cell senescence via maintaining mitochondrial homeostasis

Project description:Although the mTOR-4E-BP1 signaling pathway is implicated in aging and aging-related disorders, the role of 4E-BP1 in regulating human stem cell homeostasis remains largely unknown. Here, we report that the expression of 4E-BP1 decreases along with the senescence of human mesenchymal stem cells (hMSCs). Genetic inactivation of 4E-BP1 in hMSCs accelerates cellular senescence, compromises mitochondrial respiration and increases mitochondrial ROS production. Mechanistically, the absence of 4E-BP1 destabilizes proteins in mitochondrial respiration complexes, especially several key subunits of the complex III including UQCRC2. Ectopic expression of 4E-BP1 attenuates mitochondrial abnormalities and alleviates cellular senescence in 4E-BP1-deficient hMSCs as well as in physiologically aged hMSCs. These findings together demonstrate that 4E-BP1 functions as a geroprotector to alleviate human stem cell senescence and maintain mitochondrial homeostasis, particularly for the mitochondrial respiration complex III and provide a new potential target to counteract human stem cell senescence.

2023-05-10 | PXD033301 | Pride

The P-body protein 4E-T regulates the balance between cell genesis and establishment of the postnatal neural stem cell pool by repressing mRNA translation [4ET_VSVZ]

Project description:To investigate the targets of 4E-T in the postnatal V-SVZ We performed RNA immunoprecipitations (RIPseq) on V-SVZ lysates anti-4E-T or control anti-IgG antibodies, isolated and sequenced the resulting RNA

2024-02-08 | GSE224897 | GEO

Leptospira borgpetersenii str. 4E

Project description:Leptospira borgpetersenii str. 4E Genome sequencing

| PRJNA82339 | ENA

4E-BP1-dependent translation in microglia controls mechanical hypersensitivity

Project description:Spinal microglia play a pivotal role in the development of neuropathic pain. Peripheral nerve injury induces changes in the transcriptional profile of microglia, including increased expression of components of translational machinery. Whether microglial protein synthesis is stimulated following nerve injury and has a functional role in mediating pain hypersensitivity is unknown. Here, we show that nascent protein synthesis is upregulated in spinal microglia following peripheral nerve injury. Stimulating mRNA translation in microglia, via selective ablation of the translational repressor, eukaryotic initiation factor 4E-binding protein 1 (4E-BP1), promoted the transition of microglia to a reactive state and induced mechanical hypersensitivity. Conversely, inhibiting microglial translation by expressing mutant 4E-BP1 in microglia attenuated their peripheral nerve injury-induced activation and alleviated neuropathic pain. Thus, the stimulation of 4E-BP1-dependent translation promotes microglia reactivity and mechanical hypersensitivity, whereas its inhibition alleviates neuropathic pain.

2024-01-31 | GSE254472 | GEO

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