MAF1 is a chronic repressor of RNA polymerase III transcription in the mouse.

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Version: Final published version
License: CC BY 4.0
Serval ID
serval:BIB_66A30385CDCC
Type
Article: article from journal or magazin.
Collection
Publications
Institution
Title
MAF1 is a chronic repressor of RNA polymerase III transcription in the mouse.
Journal
Scientific reports
Author(s)
Bonhoure N., Praz V., Moir R.D., Willemin G., Mange F., Moret C., Willis I.M., Hernandez N.
ISSN
2045-2322 (Electronic)
ISSN-L
2045-2322
Publication state
Published
Issued date
20/07/2020
Peer-reviewed
Oui
Volume
10
Number
1
Pages
11956
Language
english
Notes
Publication types: Journal Article
Publication Status: epublish
Abstract
Maf1 <sup>-/-</sup> 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 <sup>-/-</sup> 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.
Pubmed
Open Access
Yes
Create date
24/07/2020 14:08
Last modification date
30/12/2020 7:24
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