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Genetics, Vol. 168, 867-875, October 2004, Copyright © 2004
doi:10.1534/genetics.104.027417
Cyclin D Does Not Provide Essential Cdk4-Independent Functions in Drosophila
Jan Emmerich*,
Claas A. Meyer*,
Aida Flor A. de la Cruz
,
Bruce A. Edgar and
Christian F. Lehner*,1
* Bayreuther Zentrum für Molekulare Biowissenschaften, Department of Genetics, University of Bayreuth, 95440 Bayreuth, Germany
Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, Washington 98109
1 Corresponding author: BZMB, Department of Genetics, University of Bayreuth, Universitätsstr. 30, 95447 Bayreuth, Germany.
E-mail: chle{at}uni-bayreuth.de
The three mammalian D-type cyclins are thought to promote progression through the G1 phase of the cell cycle as regulatory subunits of cyclin-dependent kinase 4 and 6. In addition, they have been proposed to control the activity of various transcription factors without a partner kinase. Here we describe phenotypic consequences of null mutations in Cyclin D, the single D-type cyclin gene in Drosophila. As previously observed with null mutations in the single Drosophila Cdk4 gene, these mutations do not primarily affect progression through the G1 phase. Moreover, the apparently indistinguishable phenotypes of double (CycD and Cdk4) and single mutants (CycD or Cdk4) argue against major independent functions of Cyclin D and Cdk4. The reduced cellular and organismal growth rates observed in both mutants indicate that Cyclin D-Cdk4 acts as a growth driver.
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