Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

18S rRNA methyltransferase EMG1 non-enzymatically influence m6A in mRNA

ABSTRACT: Defects in ribosome biogenesis can trigger a battery of cellular events to alter gene expression and cell growth. 18S rRNA methyltransferase EMG1 is an important assembly factor in ribosome biogenesis. Here, we report that downregulation of EMG1 non-enzymatically leads to decreased N6-methyladensine (m6A) levels in polyadenylated RNA. We revealed the identities of the messenger RNAs with decreased m6A intensities upon EMG1 deficiency using m6A-IP-seq. This group of mRNAs significantly overlap with the CLIP targets of IGF2BP3, which is an m6A reader protein stabilizing m6A-containing transcripts. Furthermore, both RNA-seq and qRT-PCR results suggest that the expression level of this group of mRNAs significantly decreased upon EMG1 deficiency, possibly through the regulation of IGF2BP3. Gene ontology analysis suggests that this group of mRNAs function in a list of cell signaling pathways important for cell growth. These findings collectively suggest that decreased ribosome assembly may influence gene expression via decreasing m6A levels in mRNAs.

ORGANISM(S): Mus musculus

PROVIDER: GSE190945 | GEO | 2023/12/15

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Arabidopsis HOT3/eIF5B1 constrains rRNA RNAi by facilitating 18S rRNA maturation during translation initiation (18S END-Seq)

Project description:Ribosome biogenesis is essential for protein synthesis in gene expression. Yeast eIF5B has been shown biochemically to facilitate 18S rRNA 3’ end maturation during late-40S ribosomal subunit assembly and gate the transition from translation initiation to elongation. But the effects of eIF5B have not been studied at the genome-wide level in any organism, and 18S rRNA 3’ end maturation is poorly understood in plants. Arabidopsis HOT3/eIF5B1 was found to promote development and heat-stress acclimation by translational regulation, but its molecular function remained unknown. Here, we show that HOT3 is a late-stage ribosome biogenesis factor that facilitates 18S rRNA 3’ end processing and is a translation initiation factor that globally impacts the transition from initiation to elongation. By developing and implementing 18S-ENDseq, we revealed previously unknown events in 18S rRNA 3’ end maturation or metabolism. We quantitatively defined new processing hotspots and identified adenylation as the prevalent non-templated RNA modification at the 3’ ends of pre-18S rRNAs. Aberrant 18S rRNA maturation in hot3 further activated RNAi to generate RDR1- and DCL2/4-dependent risiRNAs mainly from a 3’ portion of 18S rRNA. We further showed that risiRNAs in hot3 were predominantly localized in ribosome-free fractions not responsible for the 18S rRNA maturation or translation initiation defects in hot3. Our study uncovered the molecular function of HOT3/eIF5B1 in 18S rRNA maturation at the late-40S assembly stage and revealed the regulatory crosstalk among ribosome biogenesis, mRNA translation initiation, and siRNA biogenesis in plants.

2023-04-19 | GSE223167 | GEO

Arabidopsis HOT3/eIF5B1 constrains rRNA RNAi by facilitating 18S rRNA maturation during translation initiation (miRNA-Seq)

2023-04-19 | GSE223171 | GEO

Arabidopsis HOT3/eIF5B1 constrains rRNA RNAi by facilitating 18S rRNA maturation during translation initiation (RNA-Seq)

2023-04-19 | GSE223169 | GEO

Arabidopsis HOT3/eIF5B1 constrains rRNA RNAi by facilitating 18S rRNA maturation during translation initiation (Ribo-Seq)

2023-04-19 | GSE223168 | GEO

VIRMA-mediated m6A modification regulates forebrain formation through facilitating ribosome biogenesis

Project description:N6-methyladenosine (m6A) modification plays crucial roles in tissue development and homeostasis. However, the mechanisms underlying cellular adaptation of m6A modification and their impact on protein synthesis machinery remain unclear. VIRMA, the largest and evolutionarily conserved core of the m6A methyltransferase complex, is highly expressed in the embryonic brain and various cancers. Here, we demonstrate that VIRMA-mediated m6A modification is essential for active ribosome biogenesis. VIRMA depletion destabilizes the entire writer complex and reduces m6A levels, leading to decreased proliferation and increased apoptosis of neural progenitor/stem cells (NPCs), ultimately causing severe forebrain developmental defects. Mechanistically, VIRMA depletion impairs ribosome biogenesis by inhibiting mRNA decay, triggering a p53-dependent stress response and compromising global protein synthesis. Importantly, these findings extend to human cancer cells, suggesting a potential conservation of this mechanism. Overall, our study reveals the critical role of m6A in adapting protein synthesis machinery during brain development and potentially in cancer.

2024-10-31 | GSE279609 | GEO

VIRMA-mediated m6A modification regulates forebrain formation through facilitating ribosome biogenesis

2024-10-29 | GSE279759 | GEO

18S rRNA N6-methyladenosine (m6A) modification promotes tumorigenesis and chemoresistance via gain-of-function mutant p53 in nasopharyngeal carcinoma

Project description:Mis-regulated mRNA translation and hyperactivation of ribosome biogenesis are the two main hallmarks of cancer cells, whereas their intrinsic links and molecular mechanisms remain poorly understood. Our current study revealed that METTL5 and its mediated 18S rRNA N6-methyladenosine modification at 1832 position (m6A1832) are elevated in nasopharyngeal carcinoma (NPC) and correlated with disease progression. Gain-of-function and loss-of-function assays showed that METTL5 mediated 18S rRNA m6A1832 modification promotes NPC cells proliferation and metastasis in vitro and in vivo. Mechanistically, loss of 18S rRNA m6A1832 modification impairs the assembly of 80S ribosome and therefore affecting global mRNA translation. Furthermore, polyribosome-bound mRNA sequencing (Polyribosome-RNA-seq), ribosome profiling sequencing (Ribo-seq) and whole exome sequencing (WES) data identified a METTL5/HSF4b/HSP90B1/mutant p53 (mutp53) axis which contributed to NPC tumorigenesis and chemoresistance. Our findings uncovered a novel mechanism underlying rRNA epigenetic modification in regulating mRNA translation and mutp53 pathway in cancer.

2024-10-24 | GSE186485 | GEO

Pseudouridine-dependent ribosome biogenesis selectively regulates translation of polyglutamine proteins during Drosophila oogenesis [pulldown]

Project description:Stem cells in many systems, including Drosophila germline stem cells (GSCs), have increased ribosome biogenesis and translation during terminal differentiation. Here, we show that pseudouridylation of ribosomal RNA (rRNA) mediated by the H/ACA box is required for ribosome biogenesis and oocyte specification. Reducing ribosome levels during differentiation decreased the translation of a subset of mRNAs that are enriched for CAG repeats and encodes polyglutamine-containing proteins, including differentiation factors such as RNA-binding Fox protein 1. Moreover, ribosomes were enriched at CAG repeats within transcripts during oogenesis. Increasing TOR activity to elevate ribosome levels in H/ACA box-depleted germlines suppressed the GSC differentiation defects, whereas germlines treated with the TOR inhibitor rapamycin had reduced levels of polyglutamine-containing proteins. Thus, ribosome biogenesis and ribosome levels can control stem cell differentiation via selective translation of CAG repeat-containing transcripts.

2023-11-22 | GSE206691 | GEO

Pseudouridine-dependent ribosome biogenesis selectively regulates translation of polyglutamine proteins during Drosophila oogenesis [polysome-seq]

2023-11-22 | GSE206690 | GEO

Regulation of highly expressed hCINAP on translatome

Project description:hCINAP is essential for human 18S rRNA processing and ribosome assembly. hCINAP is highly expressed in human cancers and promotes cancer cell growth. To connect the role of hCINAP in ribosome biogenesis and tumor growth, genome-wide polysome profiling was performed to detect the regulation of hCINAP on ribosome assembly and translation control. The results showed taht hihgly expressed hCINAP promotes ribosome biogenesis and selectively modulates cancer-associated translatome to promote malignancy. This result provides important insights into the molecular mechanism underlying the role of hCINAP in tumorigenesis.

2016-07-18 | GSE81469 | GEO

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