Phosphorylation of Bicoid on MAP-kinase sites

Polarity along the anteroposterior axis of the Drosophila embryo is established by the activity of maternal gene products deposited into the egg during oogenesis. These activities direct specialised domains of zygotic gene expression required for the determination of cell fate (St. Johnston and Nüsslein-Volhard, 1992). The anterior system, which is required for the formation of the head and the thorax, is dependent on the activity of the Bicoid (Bcd) maternal morphogen (Frohnhöfer and NüssleinVolhard, 1986). Maternal bcd mRNA is localised at the anterior tip of the egg (Berleth et al., 1988). Its protein product is translated upon egg laying and diffuses along the anteroposterior axis of the syncytial blastoderm to form a concentration gradient (Driever and Nüsslein-Volhard, 1988a,b). The Bcd protein is a homeodomain (HD)-containing transcription factor that differentially activates target genes in distinct anterior domains. It has been proposed that Bcd zygotic targets respond to different threshold levels of the protein, depending on the affinity of Bcd binding sites in their promoters (Driever and Nüsslein-Volhard, 1989; Struhl et al., 1989; Gao and Finkelstein, 1998). The localised expression of Bcd targets in distinct domains is an example of how a morphogen can control pattern formation at the transcriptional level, depending on its concentration. In addition to activating transcription of its targets, Bcd has also been implicated in the translational suppression of maternal caudal (cad) mRNA. The Bcd HD that mediates DNA binding to the promoter of Bcd target genes also mediates binding of the Bcd protein to the 3′UTR of cad mRNA (Rivera-Pomar et al., 1996; Dubnau and Struhl, 1996; Chan and Struhl, 1997). Patterning of the terminal regions of the embryo is achieved by transfer of spatial information from the follicle cells to the oocyte and is mediated by activation of the Torso (Tor) signal transduction pathway. The Tor receptor tyrosine kinase (RTK) is evenly distributed at the surface of the embryo. Its restricted activation at the poles depends on factors encoded by the Nasrat, pole hole, trunk and torso-like genes. These products act upstream of the Tor RTK and they are likely to play key roles in production and accessibility of the Tor ligand (Furriols et al., 1998). Once the Tor RTK is activated, the signal is transduced by the conserved Ras signalling module (Perrimon 279 Development 127, 279-289 (2000) Printed in Great Britain © The Company of Biologists Limited 2000 DEV5324