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First published online 29 June 2004
doi: 10.1242/jcs.01240
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Research Article |

,¶Department of Zoology, University of Oxford, South Parks Road, Oxford OX1 3PS, UK
¶ Author for correspondence (e-mail: renault{at}saturn.med.nyu.edu)
Accepted 25 March 2004
Mutation of the Drosophila maternal cell cycle regulator, Gnu, results in loss of embryonic mitosis and the onset of excessive nuclear DNA replication. The Gnu phosphoprotein is normally synthesized in nurse cells and transported to the developing oocyte. We created a gnuGFP-bcd3'UTR transgene using the gnu promoter and bicoid 3'UTR, that translates GnuGFP only on egg activation from a localized anterior source. This transgene was able to rescue the sterility of gnu mutant females. Gnu is therefore first required after egg activation for polar body condensation and zygotic mitoses. Embryos containing pronounced anterior-posterior gradients of Gnu activity demonstrate that Gnu regulates mitotic activity by promoting cyclin B stability. Our gnuGFP-bcd3'UTR vector provides a novel experimental strategy to analyse the temporal requirement and role of cell cycle regulators including potential sperm-supplied factors in eggs and embryos.
Key words: Cyclin, Mitosis, Fertilisation, Drosophila melanogaster, Oocyte
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