Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

TRAP sequencing of D1 and D2 spiny projection neurons from young and old mice and ribosome profiling in NIH-3T3 cells

ABSTRACT: Particular brain regions and cell populations exhibit increased susceptibility to aging-related stresses. Here, we describe the age-specific and brain-region-specific accumulation of ribosome-associated 3' UTR RNAs that lack the 5' UTR and open reading frame. Our study reveals this phenomenon impacts hundreds of genes in aged D1 spiny projection neurons of the mouse striatum and also occurs in the aging human brain. Isolated 3' UTR accumulation is tightly correlated with mitochondrial gene expression and oxidative stress, with full-length mRNA expression that is reduced but not eliminated and with production of short 3' UTR-encoded peptides. Depletion of the oxidation-sensitive Fe-S cluster ribosome recycling factor ABCE1 induces the accumulation of 3' UTRs, consistent with a model in which ribosome stalling and mRNA cleavage by No-Go decay yields isolated 3' UTR RNAs protected by ribosomes. Isolated 3' UTR accumulation is a hallmark of brain aging, likely reflecting regional differences in metabolism and oxidative stress.

ORGANISM(S): Mus musculus

PROVIDER: GSE97461 | GEO | 2017/08/30

SECONDARY ACCESSION(S): PRJNA381914

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

RNA-seq of ABCE1-knockout cells

Project description:Nonsense-mediated decay (NMD) is a pathway that degrades messenger RNAs containing premature termination codons. Here, a genome-wide screen for NMD factors uncovered an unexpected mechanism that broadly governs 3ʹ untranslated region (UTR)-directed regulation. The screen revealed that NMD requires lysosomal acidification, which allows transferrin-mediated iron uptake, which in turn is necessary for iron-sulfur (Fe-S) cluster biogenesis. This pathway converges on the Fe-S cluster-containing ribosome recycling factor ABCE1, whose impaired function results in the movement of ribosomes into 3ʹ UTRs where they displace exon junction complexes, thereby abrogating NMD. Importantly, these effects extend beyond NMD substrates, with ABCE1 activity required to maintain the accessibility of 3ʹ UTRs to diverse regulators, including microRNAs and RNA binding proteins. Due to the sensitivity of the Fe-S cluster of ABCE1 to iron availability and reactive oxygen species, these findings reveal an unanticipated vulnerability of 3ʹ UTR-directed regulation to lysosomal dysfunction, iron deficiency, and oxidative stress.

2020-07-14 | GSE144164 | GEO

Ribosome profiling of ABCE1-knockout cells

2020-07-14 | GSE144163 | GEO

CRISPR screen for NMD regulators

2020-07-14 | GSE144162 | GEO

RNA-seq of Paraquat-treated cells

2020-07-14 | GSE150524 | GEO

RNA-seq of Bafilomycin-treated cells

2020-07-14 | GSE150523 | GEO

Ribosome profiling of human platelets, reticulocytes, and in vitro cell lines

Project description:Translation is a fundamental biological process and ribosomes are essential in all cells, but defects in ribosome biogenesis (ribosomopathies) disproportionately cause hematopoietic dysfunction of red blood cells and platelets. Here, we analyze translation in primary human reticulocytes and platelets by ribosome profiling and uncover dramatic accumulation of post-termination, unrecycled ribosomes in the 3´UTRs of mRNAs. We then demonstrate that these ribosomes accumulate as a result of the natural loss of the ribosome recycling factor ABCE1 during terminal differentiation. We find that induction of ribosome rescue factors PELO and HBS1L is required to maintain translational homeostasis when ABCE1 levels fall. This activation of ribosome rescue mitigates the effects of ribosome shortage on translational output, including on hemoglobin production. Our observations suggest that this distinctive loss of ABCE1 in anucleate blood lineages sensitizes them to defects in ribosome homeostasis and that activation of a ribosome rescue pathway plays a lineage-specific role in maintaining ribosome homeostasis during blood cell development.

2016-09-29 | GSE85864 | GEO

Ribosome profiling study of rli1 depeletion strain

Project description:ABCE1/Rli1 functions as a ribosome recycling factor in vitro, but has not been shown to be crucial for recycling in vivo. We use ribosome profiling and biochemistry to define the role of Rli1 in living yeast. When Rli1 levels were diminished, 80S ribosomes accumulated at stop codons and, surprisingly, in the adjoining 3'UTRs of most genes. While ribosomes did not show preference for any reading frame in the 3'UTR, their enrichment at stop codons and His codons after histidine starvation is consistent with aberrant 3'UTR translation. Predicted 3'UTR translation products were detected by Western analysis and mass spectrometry, and their small sizes indicate a reinitiation mechanism. Eliminating ribosome-rescue factor Dom34 dramatically increases 3'UTR ribosome occupancy in Rli1 depleted cells, indicating that Dom34 clears the bulk of unrecycled ribosomes. Thus, Rli1 is crucial for ribosome recycling in vivo and for overall gene expression as it controls ribosome homeostasis and 3'UTR translation.

2015-06-02 | GSE69414 | GEO

Ribosome profiling under ABCE1 depletion to study aberrant translation termination

Project description:We report the effect of siRNA-mediated ABCE1 KD in HeLa cells, using a modified ribosome profiling protocol adapted from Ingolia et al., 2011 in order to specifically investigate ABCE1 role on translation termination

2020-06-30 | GSE143301 | GEO

Ribosome profiling of ABCE1-knockout cells

Project description:Ribosome profiling of ABCE1-knockout cells

| PRJNA602917 | ENA

Integrated genome and proteome-wide analysis reveals organ-specific proteome deterioration during aging in rat

Project description:RNA-Seq and ribosome profiling describes changes in gene expression during aging RNA-Seq and ribosome profiling from matched young and old rat liver and brain

2015-09-22 | E-GEOD-66715 | biostudies-arrayexpress

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data