Journal
EMBO JOURNAL
Volume 31, Issue 8, Pages 1916-1930Publisher
WILEY
DOI: 10.1038/emboj.2012.33
Keywords
Drosophila growth; insulin; RNA polymerase III; TOR
Categories
Funding
- Canadian Institutes of Health Research (CIHR) [MOP-86622]
- Alberta Cancer Foundation
- Alberta Innovates Health Solutions
- Natural Sciences and Engineering Research Council of Canada
- Alberta Children's Hospital Research Institute for Child and Maternal Health
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The nutrient/target-of-rapamycin (TOR) pathway has emerged as a key regulator of tissue and organismal growth in metazoans. The signalling components of the nutrient/TOR pathway are well defined; however, the downstream effectors are less understood. Here, we show that the control of RNA polymerase (Pol) III-dependent transcription is an essential target of TOR in Drosophila. We find that TOR activity controls Pol III in growing larvae via inhibition of the repressor Maf1 and, in part, via the transcription factor Drosophila Myc (dMyc). Moreover, we show that loss of the Pol III factor, Brf, leads to reduced tissue and organismal growth and prevents TOR-induced cellular growth. TOR activity in the larval fat body, a tissue equivalent to vertebrate fat or liver, couples nutrition to insulin release from the brain. Accordingly, we find that fat-specific loss of Brf phenocopies nutrient limitation and TOR inhibition, leading to decreased systemic insulin signalling and reduced organismal growth. Thus, stimulation of Pol III is a key downstream effector of TOR in the control of cellular and systemic growth. The EMBO Journal (2012) 31, 1916-1930. doi: 10.1038/emboj.2012.33; Published online 24 February 2012 Subject Categories: signal transduction; development
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