Control of a Genetic Regulatory Network by a Selector Gene

Abstract

The formation of many complex structures is controlled by a special class of transcription factors encoded by selector genes. It is shown that SCALLOPED, the DNA binding component of the selector protein complex for the Drosophila wing field, binds to and directly regulates the cis-regulatory elements of many individual target genes within the genetic regulatory network controlling wing development. Furthermore, combinations of binding sites for SCALLOPED and transcriptional effectors of signaling pathways are necessary and sufficient to specify wing-specific responses to different signaling pathways. The obligate integration of selector and signaling protein inputs on cis-regulatory DNA may be a general mechanism by which selector proteins control extensive genetic regulatory networks during development.

A novel partner of Scalloped regulates Hippo signaling via antagonizing Scalloped-Yorkie activity

“…It has been shown previously that Sd acts in conjunction with Vestigial (Vg) and other transcription factors to promote wing development by directly regulating the expression of wing patterning genes [42,43]. In addition to its expression in wing discs as Vg, Sd is also expressed in other tissues and plays a broader role than Vg during development.…”

The Drosophila wing differentiation factor Vestigial–Scalloped is required for cell proliferation and cell survival at the dorso-ventral boundary of the wing imaginal disc

“…27,50,51 Interactions between vg and genes like Notch, wg and dpp would influence gene expression patterns to promote wing identity. 28 However, some authors recently concluded that vg is not a 'master gene' but a component of the genetic combination that drives wing blade development.…”

Three habits of highly effective signaling pathways: principles of transcriptional control by developmental cell signaling

“…Response elements for the Notch, Hh, TGF-␤, RTK, Wnt, and nuclear receptor pathways have been tested for sufficiency in this manner (Antoniewski et al 1996;Riese et al 1997;Xu et al 1998;Hepker et al 1999;Barolo et al 2000;Furriols and Bray 2001;Guss et al 2001;Koide et al 2001;Martin et al 2001). In general, these reporter constructs are expressed in very weak and restricted patterns, or not at all, in vivo.…”

“…For example, multimerized Su(H) binding sites (i.e., Notch response elements) fail to drive significant reporter gene expression in Notch-responding cells in transgenic Drosophila ( Fig. 2A; Guss et al 2001). The vertebrate Su(H) ortholog CBF1 has been tested for sufficiency in transgenic mice, with similar results: A GFP reporter construct containing eight CBF1 binding sites (Hsieh et al 1996) is not activated in Notch-responsive thymocytes in vivo (S.M.…”