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Molecular and Cellular Biology, September 2001, p. 5806-5814, Vol. 21, No. 17
Division of Molecular Biology of the Cell II, German Cancer
Research Centre, D-69120 Heidelberg,
Germany1; Institute of Biomedical
and Life Sciences, Division of Biochemistry and Molecular Biology,
University of Glasgow, Glasgow G12 8QQ, United
Kingdom2; and The Netherlands Cancer
Institute, Division of Molecular Biology, 1066 CX Amsterdam, The
Netherlands3
Received 5 February 2001/Returned for modification 9 March
2001/Accepted 7 May 2001
The "pocket" proteins pRb, p107, and p130 are a family of
negative growth regulators. Previous studies have demonstrated that overexpression of pRb can repress transcription by RNA polymerase (Pol)
I. To assess whether pRb performs this role under physiological conditions, we have examined pre-rRNA levels in cells from mice lacking
either pRb alone or combinations of the three pocket proteins. Pol I
transcription was unaffected in pRb-knockout fibroblasts, but specific
disruption of the entire pRb family deregulated rRNA synthesis. Further
analysis showed that p130 shares with pRb the ability to repress Pol I
transcription, whereas p107 is ineffective in this system. Production
of rRNA is abnormally elevated in Rb
0270-7306/01/$04.00+0 DOI: 10.1128/MCB.21.17.5806-5814.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.
Overlapping Functions of the pRb Family in the
Regulation of rRNA Synthesis
/
p130
/
fibroblasts. Furthermore, overexpression
of p130 can inhibit an rRNA promoter both in vitro and in vivo. This
reflects an ability of p130 to bind and inactivate the upstream binding
factor, UBF. The data imply that rRNA synthesis in living cells is
subject to redundant control by endogenous pRb and p130.
*
Corresponding author. Mailing address: Division of
Molecular Biology of the Cell II, German Cancer Research Centre, Im
Neuenheimer Feld 280, D-69120 Heidelberg, Germany. Phone:
49-6221-423-441. Fax: 49-6221-423-404. E-mail:
r.voit{at}dkfz-heidelberg.de.
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