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GENES & DEVELOPMENT 18:2602-2607, 2004
©2004 by Cold Spring Harbor Laboratory Press; ISSN 0890-9369/ $5.00
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RESEARCH COMMUNICATION

Skp2-dependent degradation of p27kip1 is essential for cell cycle progression

Uta Kossatz1,2, Nils Dietrich1,2, Lars Zender1, Jan Buer3, Michael P. Manns1 and Nisar P. Malek1,2,4

1 Department of Gastroenterology, Hepatology and Endocrinology and 2 Institute for Molecular Biology, Hannover Medical School, Hannover, Germany; 3 Gesellschaft für Biotechnologische Forschung, Braunschweig, Germany

The activity of the SCFskp2 E3 ligase is required for the proteolytic turnover of several proteins involved in cell cycle control and transcriptional regulation. Loss of skp2 in the mouse leads to a complex phenotype including changes in cell size and DNA content as well as severe proliferation defects. Here we show that the loss of a single skp2 substrate, namely, the cyclin kinase inhibitor p27kip1, reverts the phenotype of skp2 knockout hepatocytes to normal. By comparing the kinetics of p27 turnover and cell cycle progression in skp2 knockout and p27T187A knock-in mice, we define a short period in G1 in which p27 is able to block the cell cycle after the exit from quiescence. Loss of p27 turnover during this period prevents mitotic division and instead leads to compensatory cell growth.

[Keywords: p27kip1; skp2; proteolysis; cell size; proliferation]

Received May 5, 2004; revised version accepted September 1, 2004.

Supplemental material is available at http://www.genesdev.org.

Article and publication are at http://www.genesdev.org/cgi/doi/10.1101/gad.321004.

4 Corresponding author.
E-MAIL Malek.Nisar{at}MH-Hannover.de; FAX 01149-511-532-4283.


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