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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 [Cpeb4_VSVZ]

ABSTRACT: To investigate the targets of Cpeb4 in the postnatal V-SVZ We performed RNA immunoprecipitations (RIPseq) on V-SVZ lysates anti-Cpeb4 or control anti-IgG antibodies, isolated and sequenced the resulting RNA

ORGANISM(S): Mus musculus

PROVIDER: GSE224896 | GEO | 2024/02/08

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 [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

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]

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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]

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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

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

2024-02-08 | GSE224857 | 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.

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Cpeb4-mediated Translational Regulatory Circuitry Controls Terminal Erythroid Differentiation

Project description:Erythropoiesis is essential to mammals and is regulated at multiple steps by both extracellular and intracellular factors. Many transcriptional regulatory networks in erythroid differentiation have been well characterized. However, our understanding of post-transcriptional regulatory circuitries in this developmental process is still limited. Using genomic approaches, we identified a sequence-specific RNA-binding protein, Cpeb4, which is dramatically induced in terminal erythroid differentiation (TED) by two erythroid important transcription factors, Gata1/Tal1. Cpeb4 belongs to the cytoplasmic polyadenylation element binding (CPEB) protein family that regulates translation of target mRNAs in early embryonic development, neuronal synapse, and cancer. Using primary mouse fetal liver erythroblasts, we found that Cpeb4 is required for terminal erythropoiesis by repressing the translation of a set of mRNAs highly expressed in progenitor cells. This translational repression occurs by the interaction with a general translational initiation factor, eIF3. Interestingly, Cpeb4 also binds its own mRNA and represses its translation, thus forming a negative regulatory circuitry to limit Cpeb4 protein level. This mechanism ensures that the translation repressor, Cpeb4, does not interfere with the translation of other mRNAs in differentiating erythroblasts. Our study characterized a translational regulatorycircuitry that controls TED and revealed that Cpeb4 is required for somatic cell differentiation. We used microarray to identify mRNAs associated with Cpeb4 in mouse fetal liver erythroblasts. Cpeb4 associated mRNAs were isolated from mouse fetal liver erythroblasts using anti-Cpeb4 antibody for immunoprecipitation followed by RNA extraction. Then Affymetrix microarrays were used to identify and quantify the mRNAs associated with Cpeb4.

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

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Adult mouse choroid plexus OTX2 Co-IP

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2021-08-23 | PXD021244 | Pride

RNA immunoprecipitation to identify RHA-binding transcripts in HEK293 cells

Project description:Given that RHA regulates translation by binding a PCE located at the 5’ UTR of the target transcripts a genome-wide screen was performed to identify mRNAs that bind RHA in vivo. The results from four experiments with samples obtained in four independent RNA immunoprecipitations identified 375 transcripts that co-immunoprecipitate with FLAG RHA. Since N-terminal FLAG tagged RHA specifically co-immunoprecipitates PCE-containing mRNAs HEK293 cells were transfected with a CMV-FLAG-RHA construct. Cytoplasmic lysates were immunoprecipitated with anti-FLAG beads. RNA was extracted from the immunoprecipitate and used to probe a human Agilent expression arrays. An immunoprecipitation with cells transfected with empty FLAG plasmid was used as negative control.

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