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Ribosome-profiling experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”

ABSTRACT: Ribosome-profiling experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”

PROVIDER: PRJNA412979 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR6128380.fastq.gz	Fastqsanger.gz
	SRR6128390.fastq.gz	Fastqsanger.gz
	SRR6128381.fastq.gz	Fastqsanger.gz
	SRR6128391.fastq.gz	Fastqsanger.gz
	SRR6128382.fastq.gz	Fastqsanger.gz

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Ribosome-profiling experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”

Project description:To characterize the translation defects in Maf1-/- samples, we used ribosome profiling on three WT and three Maf1-/- fed livers. Each sample was spiked with a fixed amount of Drosophila S2 Schneider cell material as an internal control for sample-to-sample normalization, and to allow detection of global changes in translation.

2019-11-04 | GSE104503 | GEO

Affymetrix experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”

Project description:Affymetrix experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”

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ChIP-seq experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”

Project description:ChIP-seq experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”

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ChIP-seq experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”

Project description:To characterize the PolIII transcription changes in Maf1-/- samples, we perfomeded ChIP-seq on WT and Maf1-/- Mouse liver samples. Mice were either fasted during eight hours or fasted for four hours and then refed.

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Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance

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RNA-seq total KO experiments for "Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance"

Project description:RNA-seq total KO experiments for "Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance"

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RNA-seq total KO experiments for "Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance"

Project description:To examine the effect of MAF1 on the RNA polymerase II transcriptome, RNA-seq was performed on samples of liver from overnight fasted and four hour refed wild-type and whole-body Maf1-/- mice.

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Affymetrix experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”

Project description:To determine how feeding and fasting might alter transcription, we analyzed liver mRNA from wild-type fasted (WT_F) or wild-type fasted and refed (WT_R) mice by gene expression arrays.

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Contrasting effects of whole-body and hepatocyte-specific deletion of the RNA polymerase III repressor Maf1 in the mouse [ChIP-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 | GSE224916 | GEO

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

2023-11-28 | GSE224743 | GEO