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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]

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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 [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

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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.

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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.

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

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