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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE104503 | GEO | 2019/11/04

REPOSITORIES: GEO

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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.

2019-11-04 | GSE104531 | 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.

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

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

2019-11-04 | GSE104535 | 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

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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

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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Differential expression of Aspergillus genes as a result of disrupting maf1

Project description:We identified a 14-3-3 homolog (maf1) in an EST library made under conditions conducive to aflatoxin biosynthesis. Disruption of this gene in A. flavus by site directed mutagenesis abolished aflatoxin production. The maf1 mutant was morphologically similar to wild type but had reduced conidiation and growth on some media. DNA expression analysis of the wild type and maf1 mutant revealed that the mutation affected the expression profile of a set of genes associated with aflatoxin production. Keywords = Aspergillus Keywords = aflatoxin Keywords = 14-3-3 Keywords: repeat sample

2004-12-09 | GSE861 | GEO

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”

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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”

| PRJNA413121 | ENA

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

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