Dorso-ventral axis formation of the Drosophila oocyte requires Cyclin G.

In general, cyclins control the cell cycle. Not so the atypical cyclins, which are required for diverse cellular functions such as for genome stability or for the regulation of transcription and translation. The atypical Cyclin G (CycG) gene of Drosophila has been involved in the epigenetic regulation of abdominal segmentation, cell proliferation and growth, based on overexpression and RNAi studies, but detailed analyses were hampered by the lack of a cycG mutant. For further investigations, we subjected the cycG locus to a detailed molecular analysis. Moreover, we studied a cycG null mutant that we recently established. The mutant flies are homozygous viable, however, the mutant females are sterile and produce ventralized eggs. Here we show that this egg phenotype is primarily a consequence of a defective Epidermal Growth Factor Receptor (EGFR) signalling pathway. By using different read outs, we demonstrate that cycG loss is tantamount to lowered EGFR signalling. Inferred from epistasis experiments, we conclude that CycG promotes the Grk signal in the oocyte. Abnormal accumulation but regular secretion of the Grk protein suggests defects of Grk translation in cycG mutants rather than transcriptional regulation. Accordingly, protein accumulation of Vasa, which acts as an oocyte specific translational regulator of Grk in the oocyte is abnormal. We propose a role of cycG in processes that regulate translation of Grk and hence, influence EGFR-mediated patterning processes during oogenesis.