The mammalian TEF and the Drosophila scalloped genes belong to a conserved family of transcriptional factors

The growth and patterning of the Drosophila wing is dependent on the formation of compartments in the wing imaginal disc which are defined by the restricted expression of the selector genes engrailed and invected in the posterior compartment and apterous in the dorsal compartment (reviewed in Blair, 1997). Interaction between cells at the boundary of these compartments leads to the production of the signaling molecules Wingless (Wg) at the dorsoventral (DV) boundary and Decapentaplegic (Dpp) at the anteroposterior (AP) boundary and to the activation of the Notch (N) pathway at the DV boundary (Lecuit et al., 1996; Neumann and Cohen, 1996, 1997; Serrano and O’Farrell, 1997). These proteins will regulate the expression of several genes amongst which vestigial (vg) and scalloped (sd) play a crucial role in wing morphogenesis. These two genes are expressed in the wing primordia with identical patterns and mutations of both genes are associated with a loss of wing tissue. vg expression is regulated by two separate enhancers: the boundary (BE) and the quadrant enhancer (QE) (Kim et al., 1996; Williams et al., 1994). The BE directs vg expression at the DV boundary whilst the QE drives vg expression in the rest of the wing pouch. These two enhancers are sequentially activated by the DV signaling pathway (N, wg) and the AP signaling pathway (dpp) and allow vg expression in the wing pouch with highest expression at the DV boundary (Kim et al., 1996, 1997). It has been shown that ectopic vg but not sd expression, in the eye-antenna or leg imaginal discs induces wing tissue outgrowth, misexpression of wing-specific genes such as sd, drosophila serum responsive factor (dsrf), spalt (sal) and spalt related gene (salr), and its own expression (Kim et al., 1996; Halder et al., 1998; Paumard-Rigal et al., 1998; Simmonds et al., 1998). In addition, several observations demonstrate that Vg must interact directly with Sd to activate target gene expression and promote wing tissue proliferation: (i) in vitro protein interaction tests and two-hybrid experiments have shown that Vg and Sd form a dimer (Paumard-Rigal et al., 1998; Simmonds et al., 1998), (ii) trans-determination as well as gene induction associated with ectopic vg expression are suppressed in sd mutants (Paumard-Rigal et al., 1998; Simmonds et al., 1998), (iii) binding sites for Sd have been identified in the enhancers of several genes regulated by Vg and in the two vg enhancers. In S2 cells, induction of these enhancers by Vg requires the function of the Sd protein (Halder 4807 Development 126, 4807-4816 (1999) Printed in Great Britain © The Company of Biologists Limited 1999 DEV7737