Datasets

Title	Ribosome-profiling experiments for “Chronic repression by MAF1 supports futile RNA cycling as a mechanism for obesity resistance”
Organism
Number of Samples	6
Release Date	2017/10/02 00:00
Sequencing Types
Protocol Details

Title
Authors	Bonhoure N, Praz V, Moir RD, Willemin G, Mange F, Moret C, Willis IM, Hernandez N
Journal	Scientific reports
Publication Date	2020 Jul 20
Abstract	Maf1 -/- mice are lean, obesity-resistant and metabolically inefficient. Their increased energy expenditure is thought to be driven by a futile RNA cycle that reprograms metabolism to meet an increased demand for nucleotides stemming from the deregulation of RNA polymerase (pol) III transcription. Metabolic changes consistent with this model have been reported in both fasted and refed mice, however the impact of the fasting-refeeding-cycle on pol III function has not been examined. Here we show that changes in pol III occupancy in the liver of fasted versus refed wild-type mice are largely confined to low and intermediate occupancy genes; high occupancy genes are unchanged. However, in Maf1 -/- mice, pol III occupancy of the vast majority of active loci in liver and the levels of specific precursor tRNAs in this tissue and other organs are higher than wild-type in both fasted and refed conditions. Thus, MAF1 functions as a chronic repressor of active pol III loci and can modulate transcription under different conditions. Our findings support the futile RNA cycle hypothesis, elaborate the mechanism of pol III repression by MAF1 and demonstrate a modest effect of MAF1 on global translation via reduced mRNA levels and translation efficiencies for several ribosomal proteins.
PMC	PMC7371695
PMID	32686713
DOI

Bonhoure et al. 2019 (PRJNA412979)