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First published online 21 December 2006
doi: 10.1242/dev.02738

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Rbf1-independent termination of E2f1-target gene expression during early Drosophila embryogenesis

Shusaku Shibutani^1,*, Lisa M. Swanhart^1,* and Robert J. Duronio^1,2,3,

¹ Department of Biology, University of North Carolina, Chapel Hill, NC 27599, USA.
² Program in Molecular Biology and Biotechnology, University of North Carolina, Chapel Hill, NC 27599, USA.
³ Lineberger Comprehensive Cancer Center, University of North Carolina, Chapel Hill, NC 27599, USA.

Author for correspondence (e-mail: duronio{at}med.unc.edu)

Accepted 14 November 2006

The initiation and maintenance of G1 cell cycle arrest is a key feature of animal development. In the Drosophila ectoderm, G1 arrest first appears during the seventeenth embryonic cell cycle. The initiation of G1₁₇ arrest requires the developmentally-induced expression of Dacapo, a p27-like Cyclin E-Cdk2 inhibitor. The maintenance of G1₁₇ arrest requires Rbf1-dependent repression of E2f1-regulated replication factor genes, which are expressed continuously during cycles 1-16 when S phase immediately follows mitosis. The mechanisms that trigger Rbf1 repressor function and mediate G1₁₇ maintenance are unknown. Here we show that the initial downregulation of expression of the E2f1-target gene RnrS, which occurs during cycles 15 and 16 prior to entry into G1₁₇, does not require Rbf1 or p27^Dap. This suggests a mechanism for Rbf1-independent control of E2f1 during early development. We show that E2f1 protein is destroyed in a cell cycle-dependent manner during S phase of cycles 15 and 16. E2f1 is destroyed during early S phase, and requires ongoing DNA replication. E2f1 protein reaccumulates in epidermal cells arrested in G1₁₇, and in these cells the induction of p27^Dap activates Rbf1 to repress E2f1-target genes to maintain a stable G1 arrest.

Key words: Drosophila, E2F, pRb, Cell cycle, G1

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