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

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

ORGANISM(S): Mus musculus

PROVIDER: GSE104535 | GEO | 2019/11/04

REPOSITORIES: GEO

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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.

2019-11-04 | GSE104534 | GEO

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.

2019-11-04 | GSE104531 | GEO

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

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.

2019-11-04 | GSE104496 | GEO

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

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

| PRJNA413117 | ENA

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”

| PRJNA413120 | ENA

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

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

| PRJNA412979 | ENA

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”

| PRJNA413121 | ENA

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"

| PRJNA412978 | ENA

Loss of the RNA polymerase III repressor MAF1 confers obesity resistance.

Project description:MAF1 is a global repressor of RNA polymerase III transcription that regulates the expression of highly abundant noncoding RNAs in response to nutrient availability and cellular stress. Thus, MAF1 function is thought to be important for metabolic economy. Here we show that a whole-body knockout of Maf1 in mice confers resistance to diet-induced obesity and nonalcoholic fatty liver disease by reducing food intake and increasing metabolic inefficiency. Energy expenditure in Maf1(-/-) mice is increased by several mechanisms. Precursor tRNA synthesis was increased in multiple tissues without significant effects on mature tRNA levels, implying increased turnover in a futile tRNA cycle. Elevated futile cycling of hepatic lipids was also observed. Metabolite profiling of the liver and skeletal muscle revealed elevated levels of many amino acids and spermidine, which links the induction of autophagy in Maf1(-/-) mice with their extended life span. The increase in spermidine was accompanied by reduced levels of nicotinamide N-methyltransferase, which promotes polyamine synthesis, enables nicotinamide salvage to regenerate NAD(+), and is associated with obesity resistance. Consistent with this, NAD(+) levels were increased in muscle. The importance of MAF1 for metabolic economy reveals the potential for MAF1 modulators to protect against obesity and its harmful consequences.

| S-EPMC4421982 | biostudies-literature

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