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CPEB4-mediated translational regulation in ex vivo activated CD8 Tcells

ABSTRACT: CPEB4-mediated translational regulation in ex vivo activated CD8 Tcells

PROVIDER: PRJNA784433 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR17043548.fastq.gz	Fastqsanger.gz
	SRR17043549.fastq.gz	Fastqsanger.gz
	SRR17043550.fastq.gz	Fastqsanger.gz
	SRR17043551.fastq.gz	Fastqsanger.gz
	SRR17043552.fastq.gz	Fastqsanger.gz

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CPEB4-mediated translational regulation in ex vivo activated CD8 Tcells [RIP-seq]

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CPEB4-mediated translational regulation in ex vivo activated CD8 Tcells [RNA-seq]

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CPEB4-mediated translational regulation in ex vivo activated CD8 Tcells [RIP-seq]

Project description:Here we show that CPEB4 preferably binds targets related to UPR and anaolic pathways in activated CD8 T cells

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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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CPEB4-mediated translational regulation in ex vivo activated CD8 Tcells

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

2023-02-06 | GSE189766 | GEO

Cpeb4-mediated Translational Regulatory Circuitry Controls Terminal Erythroid Differentiation

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CPEB4 prevents hepatic steatosis [RNA-Seq]

Project description:The Cytoplasmic Polyadenylation Element Binding (CPEB)-family of RNA-binding proteins regulates pre-mRNA processing and translation of CPE-containing mRNAs in early embryonic development and synaptic activity. However, the specific functions of each CPEB in the adult organism are poorly understood. Here we show that CPEB4 is required to suppress high fat diet- and aging-induced endoplasmic reticulum (ER) stress, and its subsequent hepatic steatosis. Stress-activated expression of CPEB4 in the liver is controlled through a double layer of regulation. First, Cpeb4 is transcriptionally regulated by the circadian clock and then, its mRNA translation is regulated by the Unfolded Protein Response (UPR) through the upstream Open Reading Frames (uORFs) present in its 5’ UTR. Thus, CPEB4 is synthesized only upon ER-stress but the amplitude of the induction is circadian. In turn, CPEB4 activates a second wave of UPR-translation required to maintain ER and mitochondrial homeostasis. Our results suggest that combined transcriptional and translational regulation of CPEB4 generates a “circadian mediator”, which coordinates the hepatic UPR activity with periods of high ER protein-folding demand preventing non-alcoholic fatty liver disease (NAFLD).

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