The orb gene encodes an RNA recognition motif (RRM)- type RNA-binding protein that is a member of the cytoplasmic polyadenylation element binding protein (CPEB) family of translational regulators. Early in oogenesis, orb is required for the formation

mRNA localization pathways play a central role in axis determination in Drosophila (St Johnson and NussleinVolhard, 1992). The posterior axis of the embryo is specified by a Nanos (Nos) protein gradient, which is generated from the translation of nos mRNA anchored at the posterior pole (Lasko, 1999). nos mRNA is localized at the pole during oogenesis by a mechanism that depends upon the oskar (osk) gene (Ephrussi and Lehmann, 1992; Smith et al., 1992). In stage 8-10 egg chambers, osk mRNA is transported to the posterior pole of the oocyte by Staufen (Stau) (St Johnston et al., 1991; St Johnston, 1995; Theurkauf, 1994) where it is activated for translation (Rongo et al., 1995). Newly synthesized Osk protein then nucleates the assembly of structures required to localize nos mRNA and to form the pole plasm. The establishment of the dorsoventral (DV) axis of the Drosophila egg and embryo also depends upon mRNA localization (see Nilson and Schupbach, 1999; Shulman and St Johnston, 1999 for reviews). Around stage 7 of oogenesis, the microtubule network is reorganized, and the oocyte nucleus moves from the posterior of the oocyte to the dorsal-anterior corner (Theurkauf, 1994). Shortly thereafter, K(10) and squid (sqd) begin concentrating gurken (grk) mRNA, which encodes a transforming growth factor α (TGFα) homolog, in a cap just above the oocyte nucleus (Neuman-Silberberg and Schupbach, 1993; Gonzales-Reyes et al., 1995; Serano et al., 1995; Saunders and Cohen, 1999). Translation of grk mRNA in stage 9 egg chambers results in the localized production of Grk protein. Grk is secreted through the oocyte plasma membrane and it signals dorsal fate to the overlying follicle cell epithelium by interacting with the Drosophila epidermal growth factor receptor (DER; Egfr – FlyBase) (Price et al., 1989; Schejter and Shilo, 1989). Mutations in either grk or DER disrupt the DV signaling pathway, leading to the production of eggs with a ventralized chorion that either lack or have fused dorsal appendages. The mis-specification of follicle cell identity during oogenesis also disrupts embryonic development (Roth and Schupbach, 1994). Although the loss of grk activity in the developing oocyte or DER in the follicle cells results in the ventralization of the egg shell and embryo, mutations in K(10) and sqd have the opposite effect on DV polarity, giving a gain-of-function dorsalization of the egg chamber (Kelly, 1993; Neuman-Silberberg and Schupbach, 1993; Serano et al., 1995). The dorsalized phenotype arises because grk mRNA is distributed all along the anterior margin of the oocyte. Translation of the mislocalized mRNA results in the secretion of Grk protein around the entire circumference of the oocyte, and it signals dorsal fate to follicle cells on both the dorsal and ventral sides. 3169 Development 128, 3169-3177 (2001) Printed in Great Britain © The Company of Biologists Limited 2001 DEV4552