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| Status |
Public on Feb 29, 2016 |
| Title |
Sir2 mutants versus Controls at 2 weeks of age |
| Organism |
Drosophila melanogaster |
| Experiment type |
Expression profiling by high throughput sequencing
|
| Summary |
Although SIRT1 plays a central role in maintaining metabolic homeostasis, the molecular mechanisms remain unclear. Here we show that loss of the Drosophila SIRT1 homolog sir2 leads to the progressive onset of diabetic phenotypes, similar to studies of SIRT1 in mice. Sir2 function is both necessary and sufficient in the fat body to maintain peripheral insulin sensitivity. This activity is mediated by the Drosophila HNF4 nuclear receptor, which is deacetylated and stabilized through protein interactions with Sir2. This study demonstrates that the key metabolic activities of SIRT1 have been conserved through evolution and establishes HNF4 as a critical downstream target.
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| |
|
| Overall design |
4 sir2 mutant, 4 control samples, independent biological replicates
|
| |
|
| Contributor(s) |
Palu RA, Thummel CS |
| Citation(s) |
27058248 |
| Submission date |
Sep 11, 2015 |
| Last update date |
May 15, 2019 |
| Contact name |
Carl Thummel |
| E-mail(s) |
cthummel@genetics.utah.edu
|
| Organization name |
University of Utah School of Medicine
|
| Department |
Human Genetics
|
| Street address |
15 N 2030 E Rm 5200
|
| City |
SALT LAKE CITY |
| State/province |
UT |
| ZIP/Postal code |
84112 |
| Country |
USA |
| |
|
| Platforms (1) |
| GPL13304 |
Illumina HiSeq 2000 (Drosophila melanogaster) |
|
| Samples (8)
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|
| Relations |
| BioProject |
PRJNA295391 |
| SRA |
SRP063610 |
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