Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse [RNA-Seq]

ABSTRACT: Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse [RNA-Seq]

PROVIDER: PRJNA932334 | ENA |

REPOSITORIES: ENA

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	SRR23362449.fastq.gz	Fastqsanger.gz
	SRR23362450.fastq.gz	Fastqsanger.gz
	SRR23362451.fastq.gz	Fastqsanger.gz
	SRR23362452.fastq.gz	Fastqsanger.gz
	SRR23362453.fastq.gz	Fastqsanger.gz

Items per page:

1 - 5 of 29

Similar Datasets

Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse

Project description:The conserved phosphoprotein MAF1 is the main known direct repressor of RNA polymerase III (Pol III). MAF1 is phosphorylated and inactivated by the nutrient-sensing TORC1 kinase, making MAF1 a nutrient effector for Pol III transcription. MAF1 has been associated with lipid metabolism in D. melanogaster, C. elegans, and the mouse. However, whereas downregulation of Maf1 generally increases lipogenesis, Maf1-/- mice are lean even under a High Fat (HF) diet. Here we compared Maf1-/- mice fed a Chow diet with mice lacking Maf1 specifically in hepatocytes (Maf1hep-/- mice) fed either a Chow or HF diet. Unlike Maf1-/- mice, Maf1hep-/- mice become slightly heavier than control mice at an old age and much earlier under a HF diet, with increased adiposity. Liver ChIPseq, RNAseq and proteomics analyses indicate increased Pol III occupancy at Pol III genes, very few differences in mRNA accumulation, and subtle changes in protein accumulation that are consistent with increased lipogenesis. RNAseq and metabolite profiling indicate that liver phenotypes of Maf1-/- mice are strongly influenced by systemic inter-organ communication. Notable changes observed in the three phenotypically distinct cohorts include downregulation of Mouse Urinary Proteins, upregulation of Cyp2a4 expression, suggestive of an alteration of Growth Hormone levels or secretion pattern, and downregulation of Angiogenin, a phenomenon that might be directly linked to increased Pol III occupancy of tRNA genes in the main Angiogenin promoter region.

2023-11-28 | PXD040086 | Pride

Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse [RNA-Seq]

Project description:MAF1 is a nutrient-sensitive, TORC1-regulated repressor of RNA polymerase III (Pol III). MAF1 downregulation leads to increased lipogenesis in Drosophila melanogaster, Caenorhabditis elegans, and mice. However, Maf1−/− mice are lean as increased lipogenesis is counterbalanced by futile pre-tRNA synthesis and degradation, resulting in increased energy expenditure. We compared Chow-fed Maf1−/− mice with Chow- or High Fat (HF)-fed Maf1hep−/− mice that lack MAF1 specifically in hepatocytes. Unlike Maf1−/− mice, Maf1hep−/− mice become heavier and fattier than control mice with old age and much earlier under a HF diet. Liver ChIPseq, RNAseq and proteomics analyses indicate increased Pol III occupancy at Pol III genes, very few differences in mRNA accumulation, and protein accumulation changes consistent with increased lipogenesis. Futile pretRNA synthesis and degradation in the liver, as likely occurs in Maf1hep−/− mice, thus seems insufficient to counteract increased lipogenesis. Indeed, RNAseq and metabolite profiling indicate that liver phenotypes of Maf1−/− mice are strongly influenced by systemic inter-organ communication. Among common changes in the three phenotypically distinct cohorts, Angiogenin downregulation is likely linked to increased Pol III occupancy of tRNA genes in the Angiogenin promoter.

2023-11-28 | GSE224743 | GEO

Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse [ChIP-Seq]

2023-11-28 | GSE224916 | GEO

Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse

Project description:Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse

| PRJNA933113 | ENA

Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse [ChIP-Seq]

Project description:Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse [ChIP-Seq]

| PRJNA934546 | ENA

Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor <i>Maf1</i> in the mouse.

Project description:MAF1 is a nutrient-sensitive, TORC1-regulated repressor of RNA polymerase III (Pol III). MAF1 downregulation leads to increased lipogenesis in Drosophila melanogaster, Caenorhabditis elegans, and mice. However, Maf1 -/- mice are lean as increased lipogenesis is counterbalanced by futile pre-tRNA synthesis and degradation, resulting in increased energy expenditure. We compared Chow-fed Maf1 -/- mice with Chow- or High Fat (HF)-fed Maf1 hep-/- mice that lack MAF1 specifically in hepatocytes. Unlike Maf1 -/- mice, Maf1 hep-/- mice become heavier and fattier than control mice with old age and much earlier under a HF diet. Liver ChIPseq, RNAseq and proteomics analyses indicate increased Pol III occupancy at Pol III genes, very few differences in mRNA accumulation, and protein accumulation changes consistent with increased lipogenesis. Futile pre-tRNA synthesis and degradation in the liver, as likely occurs in Maf1 hep-/- mice, thus seems insufficient to counteract increased lipogenesis. Indeed, RNAseq and metabolite profiling indicate that liver phenotypes of Maf1 -/- mice are strongly influenced by systemic inter-organ communication. Among common changes in the three phenotypically distinct cohorts, Angiogenin downregulation is likely linked to increased Pol III occupancy of tRNA genes in the Angiogenin promoter.

| S-EPMC10746880 | biostudies-literature

Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse

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

2023-11-28 | GSE224917 | GEO

RNA seq after RNA pol III manipulation by Brf1 and Maf1 knockdown, Maf1 overexpression and ML60218 treatment in ST2 cells before, and during differentiation into osteoblasts

Project description:Maf1, a key repressor of RNA polymerase III-mediated transcription, has been shown to promote mesoderm formation in vitro. Here, we show, for the first time, that Maf1 plays a critical role in the regulation of osteoblast differentiation. We also found that, in contrast to MAF1 overexpression, other perturbations that repress RNA pol III transcription, including Brf1 knockdown and the chemical inhibition of RNA pol III by ML-60218, inhibited osteoblast differentiation. RNA-seq was used to determine the basis for these opposing actions on osteoblast differentiation. RNA polymerase III-dependent transcription was manipulated in ST2 stromal cells by Brf1 or Maf1 knockdown, ML-60218 treatment and MAF1 overexpression. The ST2 cells were then tested for their capacity to differentiate into osteoblasts. RNA-seq was performed on day 0, before differentiation and day 4 after differentiation medium was added. The modalities used to perturb RNA pol III transcription resulted in distinct changes gene expression, indicating that this transcription process is highly sensitive and triggers diverse gene expression programs and phenotypic outcomes. Specifically, Maf1 induced genes in ST2 cells known to promote osteoblast differentiation. Furthermore, genes that are induced during osteoblast differentiation displayed codon bias.

2022-05-20 | GSE203308 | GEO

Maf1 and repression of RNA polymerase III-mediated transcription drives adipocyte differentiation

Project description:RNA polymerase (pol) III transcribes a variety of small untranslated RNAs that are involved in essential cellular processes that include transcription, RNA processing, and translation. RNA pol III and its components are altered in various human developmental disorders, yet their roles in cell fate determination and development are poorly understood. Here we demonstrate that Maf1, a transcriptional repressor, promotes induction of mouse embryonic stem cells into mesoderm and their terminal differentiation into adipocytes. Reduced Maf1 expression in preadipocytes impairs adipogenesis while ectopic Maf1 expression in Maf1-/- deficient cells enhances differentiation. RNA pol III repression by either chemical inhibition or knockdown of Brf1, promotes adipogenesis. Altered RNA pol III-dependent transcription produces select changes in RNA pol II-derived transcripts with a significant enrichment of adipogenic gene signatures. Furthermore, RNA pol III-mediated transcription positively regulates long non-coding RNA H19 and Wnt6 expression, established adipogenesis inhibitors. Together, these studies reveal an important and unexpected function for RNA pol III-mediated transcription and Maf1 in mesoderm induction and cellular differentiation.

2018-08-14 | GSE113324 | GEO

Maf1 cooperates with progesterone receptors to repress RNA polymerase III transcription of select tRNAs

Project description:Progesterone receptors (PR) can regulate transcription by RNA Polymerase III (Pol III), which transcribes small non-coding RNAs, including all transfer RNAs (tRNAs). Previous work demonstrated that PR associates with the Pol III complex at tRNA genes and that progestins downregulate tRNA transcripts in breast tumor models. To further elucidate the mechanism of PR-mediated regulation of Pol III, we performed ChIP-seq for PR, the Pol III subunit POLR3A, the TFIIIB component Brf1, and the Pol III repressor Maf1 in breast cancer cells with or without progestin treatment. Upon progestin exposure, PR localized to approximately half of POLR3A-occupied tRNA genes, with Maf1 co-recruited to many of these PR-POLR3A sites. While progestin treatment did not significantly alter the number of tRNA genes occupied by Pol III or Brf1, Brf1 occupancy was stabilized, as indicated by increased peak amplitudes. Analysis of nascent tRNA transcription revealed a specific progestin-induced downregulation of approximately one-third of highly expressed tRNA genes. This repression was significantly reduced by Maf1 knockdown, indicating that Maf1 is necessary for PR-mediated tRNA downregulation. Additionally, PR co-immunoprecipitated with Maf1 along with Brf1 and POLR3A. Overall, these findings demonstrate a ligand-dependent PR-mediated repression of tRNA transcription through Maf1.

2025-09-29 | GSE283978 | 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