Ribosomal protein S6 kinase activity controls the ribosome biogenesis transcriptional program

Oncogene ◽  
2013 ◽  
Vol 33 (4) ◽  
pp. 474-483 ◽  
Author(s):  
C Chauvin ◽  
V Koka ◽  
A Nouschi ◽  
V Mieulet ◽  
C Hoareau-Aveilla ◽  
...  
2007 ◽  
Vol 25 (4) ◽  
pp. 209-226 ◽  
Author(s):  
Katarzyna Jastrzebski ◽  
Katherine M. Hannan ◽  
Elissaveta B. Tchoubrieva ◽  
Ross D. Hannan ◽  
Richard B. Pearson

2006 ◽  
Vol 291 (1) ◽  
pp. E115-E127 ◽  
Author(s):  
Ji Young Kim ◽  
Kristin Tillison ◽  
Jun-Ho Lee ◽  
David A. Rearick ◽  
Cynthia M. Smas

The minimal adipose phenotype of hormone-sensitive lipase (HSL)-null mice suggested that other hormonally responsive lipase(s) were present in adipocytes. Recent studies have characterized a new adipose tissue triglyceride lipase, ATGL/PNPLA2/destnutrin/iPLA2ζ/TTS2.2 (ATGL). We had previously cloned a novel adipose-enriched transcript by differential screening and recently determined its identity with murine ATGL. We report here on the regulation of ATGL by TNF-α and insulin in 3T3-L1 adipocytes and identify ATGL as a target for transcriptional activation by the key adipogenic transcription factor PPARγ. Insulin at 100 nM resulted in a marked decrease in ATGL transcript that was effectively blocked by inhibitors for PI 3-kinase and p70 ribosomal protein S6 kinase. TNF-α treatment decreased ATGL transcript in a time-dependent manner that paralleled TNF-α downregulation of PPARγ with a maximal decrease noted by 6 h. TNF-α effects on ATGL were attenuated by pretreatment with PD-98059, LY-294002, or rapamycin, suggesting involvement of the p44/42 MAP kinase, PI 3-kinase, and p70 ribosomal protein S6 kinase signals. To study transcriptional regulation of ATGL, we cloned 2,979 bp of the murine ATGL 5′-flanking region. Compared with promoterless pGL2-Basic, the −2979/+21 ATGL luciferase construct demonstrated 120- and 40-fold increases in activity in white and brown adipocytes, respectively. Luciferase reporter activities for a series of eight ATGL promoter deletions revealed that the −928/+21, −1738/+21, −1979/+21, and −2979/+21 constructs were transactivated by PPARγ. Our findings identify the novel lipase ATGL to be a target gene for TNF-α and insulin action in adipocytes and reveal that it is subject to transcriptional control by PPARγ-mediated signals.


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