scholarly journals The yeast DNA ligase geneCDC9 is controlled by six orientation specific upstream activating sequences that respond to cellular proliferation but which alone cannot mediate cell cycle regulation

1991 ◽  
Vol 19 (2) ◽  
pp. 359-364 ◽  
Author(s):  
Julia H.M. White ◽  
Anthony L. Johnson ◽  
Noel F. Lowndes ◽  
Leland H. Johnston
Yeast ◽  
1999 ◽  
Vol 15 (12) ◽  
pp. 1199-1210 ◽  
Author(s):  
E. Andaluz ◽  
A. Ciudad ◽  
J. Rubio Coque ◽  
R. Calderone ◽  
G. Larriba

2009 ◽  
Vol 17 (2) ◽  
pp. 244-256 ◽  
Author(s):  
Anton Khmelinskii ◽  
Johanna Roostalu ◽  
Helio Roque ◽  
Claude Antony ◽  
Elmar Schiebel

Nature ◽  
2000 ◽  
Vol 404 (6779) ◽  
pp. 782-787 ◽  
Author(s):  
René H. Medema ◽  
Geert J. P. L. Kops ◽  
Johannes L. Bos ◽  
Boudewijn M. T. Burgering

2005 ◽  
Vol 25 (24) ◽  
pp. 10940-10952 ◽  
Author(s):  
Zana P. Desgranges ◽  
Jinwoo Ahn ◽  
Maria B. Lazebnik ◽  
Todd Ashworth ◽  
Caleb Lee ◽  
...  

ABSTRACT The multifunctional transcription factor TFII-I is tyrosine phosphorylated in response to extracellular growth signals and transcriptionally activates growth-promoting genes. However, whether activation of TFII-I also directly affects the cell cycle profile is unknown. Here we show that under normal growth conditions, TFII-I is recruited to the cyclin D1 promoter and transcriptionally activates this gene. Most strikingly, upon cell cycle arrest resulting from genotoxic stress and p53 activation, TFII-I is ubiquitinated and targeted for proteasomal degradation in a p53- and ATM (ataxia telangiectasia mutated)-dependent manner. Consistent with a direct role of TFII-I in cell cycle regulation and cellular proliferation, stable and ectopic expression of wild-type TFII-I increases cyclin D1 levels, resulting in accelerated entry to and exit from S phase, and overcomes p53-mediated cell cycle arrest, despite radiation. We further show that the transcriptional regulation of cyclin D1 and cell cycle control by TFII-I are dependent on its tyrosine phosphorylation at positions 248 and 611, sites required for its growth signal-mediated transcriptional activity. Taken together, our data define TFII-I as a growth signal-dependent transcriptional activator that is critical for cell cycle control and proliferation and further reveal that genotoxic stress-induced degradation of TFII-I results in cell cycle arrest.


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