Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

P53 activation during ribosome biogenesis regulates normal erythroid differentiation. [ChIP-Seq]

ABSTRACT: p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [ChIP-Seq]

PROVIDER: PRJNA660447 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR12556664_1.fastq.gz	Fastqsanger.gz
	SRR12556664_2.fastq.gz	Fastqsanger.gz
	SRR12556665_1.fastq.gz	Fastqsanger.gz
	SRR12556665_2.fastq.gz	Fastqsanger.gz
	SRR12556666_1.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 8

Similar Datasets

p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [expression]

Project description:The role of ribosome biogenesis in erythroid development is supported by the recognition of erythroid defects in ribosomopathies in both Diamond-Blackfan anemia and 5q- syndrome. Whether ribosome biogenesis exerts a regulatory function on normal erythroid development is still unknown. In the present study, a detailed characterization of ribosome biogenesis dynamics during human and murine erythropoiesis shows that ribosome biogenesis is abruptly interrupted by the drop of rDNA transcription and the collapse of ribosomal protein neo-synthesis. Its premature arrest by RNA polI inhibitor, CX-5461 targets the proliferation of immature erythroblasts. We also show that p53 is activated spontaneously or in response to CX-5461 concomitantly to ribosome biogenesis arrest, and drives a transcriptional program in which genes involved in cell cycle arrest, negative regulation of apoptosis and DNA damage response were upregulated. RNA polI transcriptional stress results in nucleolar disruption and activation of ATR-CHK1-p53 pathway. Our results imply that the timing of ribosome biogenesis extinction and p53 activation are crucial for erythroid development. In ribosomopathies in which ribosome availability is altered by unbalanced production of ribosomal proteins, the threshold of ribosome biogenesis down-regulation could be prematurely reached and together with pathological p53 activation prevents a normal expansion of erythroid progenitors.

2020-09-14 | GSE137951 | GEO

p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [ChIP-Seq]

2020-09-14 | GSE157208 | GEO

p53 activation during ribosome biogenesis regulates normal erythroid differentiation.

Project description:p53 activation during ribosome biogenesis regulates normal erythroid differentiation.

| PRJNA660448 | ENA

p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [expression]

Project description:p53 activation during ribosome biogenesis regulates normal erythroid differentiation. [expression]

| PRJNA573943 | ENA

Atf4 promotes erythroid differentiation by regulating ribosome biogenesis via RPS19BP1

Project description:Atf4 promotes erythroid differentiation by regulating ribosome biogenesis via RPS19BP1

| PRJNA987998 | ENA

RNA exosome mutations in pontocerebellar hypoplasia alter ribosome biogenesis and p53 levels

Project description:The eukaryotic RNA exosome is a ubiquitously expressed complex of nine core proteins (EXOSC1-9) and associated nucleases responsible for RNA processing and degradation. Autosomal recessive mutations in EXOSC3, EXOSC8, EXOSC9 and the exosome cofactor RBM7 cause pontocerebellar hypoplasia and motor neuronopathy. To understand the importance of the exosome in neurodegeneration, we investigated the consequences of exosome mutations on RNA metabolism and cellular survival in zebrafish and human cell models. We observed that levels of mRNAs encoding p53 and ribosome biogenesis factors are upregulated in zebrafish lines with homozygous mutations of exosc8 or exosc9, respectively. In addition, exosome deficiency leads to increased levels of multiple non-coding RNAs (e.g. tRNAs, snoRNAs, scaRNAs). Consistent with higher p53 levels, mutant zebrafish have a reduced head size, smaller brain and cerebellum caused by an increased number of apoptotic cells during development. Downregulation of EXOSC9 in human cells leads to p53 protein stabilisation and G2/M cell cycle arrest. The work provides explanation for the pathogenesis of exosome-related disorders and highlights the link between exosome function, ribosome biogenesis and p53-dependent signalling.

2020-05-30 | GSE151452 | GEO

RNA exosome mutations in pontocerebellar hypoplasia alter ribosome biogenesis and p53 levels

Project description:RNA exosome mutations in pontocerebellar hypoplasia alter ribosome biogenesis and p53 levels

| PRJNA635887 | ENA

A non-canonical role for a small nucleolar RNA in ribosome biogenesis and senescence (Ribosome profiling)

Project description:Oncogene-induced senescence is an important tumor suppressor mechanism that limits proliferation of cells harboring oncogenic mutations. Through a genome-wide screen, we discovered a conserved snoRNA, SNORA13, that is required for this pathway. Although SNORA13 guides the pseudouridylation of a highly conserved nucleotide in the ribosomal decoding center, loss of this snoRNA minimally impacts translation. Instead, we found that SNORA13 negatively regulates ribosome biogenesis. Oncogenic stress perturbs ribosome biogenesis, resulting in the accumulation of free ribosomal proteins (RPs) that trigger p53 activation. We showed that SNORA13 interacts directly with RPL23, decreasing its incorporation into maturing 60S subunits and, consequently, increasing the pool of free RPs, thereby promoting the p53-mediated senescence program. Thus, SNORA13 regulates ribosome biogenesis and the p53 pathway through a non-canonical mechanism distinct from its role in guiding RNA modification. These findings expand our understanding of snoRNA functions and the roles of these abundant noncoding RNAs in cellular signaling.

2024-07-01 | GSE232858 | GEO

p53 activation during ribosome biogenesis regulates normal erythroid differentiation.

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

2020-09-14 | GSE157210 | GEO

Runx1 deficiency decreases ribosome biogenesis and confers stress resistance to hematopoietic stem and progenitor cells

Project description:The transcription factor RUNX1 is frequently mutated in myelodysplastic syndrome and leukemia. RUNX1 mutations can be early events, creating pre-leukemic stem cells that expand in the bone marrow. Here we show that, counter-intuitively, Runx1 deficient hematopoietic stem and progenitor cells (HSPCs) have a slow growth, low biosynthetic, small cell phenotype and markedly reduced ribosome biogenesis (Ribi). The reduced Ribi involves decreased levels of rRNA and many mRNAs encoding ribosome proteins. Runx1 appears to directly regulate Ribi; Runx1 is enriched on the promoters of genes encoding ribosome proteins, and binds the ribosomal DNA repeats. Runx1 deficient HSPCs have lower p53 levels, reduced apoptosis, an attenuated unfolded protein response, and accordingly are resistant to genotoxic and endoplasmic reticulum stress. The low biosynthetic activity and corresponding stress resistance provides a selective advantage to Runx1 deficient HSPCs, allowing them to expand in the bone marrow and outcompete normal HSPCs. Comparison of the phenotypic and molecular properties of normal (Runx1f/f, or WT) versus Runx1 deficient (Mut) hematopoietic stem cells.

2015-07-27 | E-GEOD-67609 | 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