A model for the combinatorial effects of Wg, Dpp, Ras1 and neurogenic signals in embryonic mesoderm development. The intersection of Wg (red) and Dpp (blue) expression domains delineates a prepattern (purple) in which L'sc is initially expressed as a precluster (green) (data). This entire precluster is competent to respond to a subsequent RTK/Ras1 signal. However, localized activation of Htl and DER restricts L'sc to a subset of precluster cells which represent an equivalence group. Further RTK/Ras1 signaling activates Eve expression in all cells of the L'sc cluster (orange). A single progenitor is determined under the lateral inhibitory influence of the neurogenic genes (pink) (data). This model applies to both the pericardial and somatic muscle Eve/L'sc clusters, both of which derive from the same precluster. For simplicity, only one cluster is shown.
From Carmena et al., Genes & Development
A model for developmental competence, signal integration and RTK/Ras response specificity in the determination of mesodermal Eve progenitors. Wg and Dpp provide competence (gray box) through the regulation of tissue-specific transcription factors (Tin, Twi), signal-responsive transcription factors (Mad, dTCF), and proximal components of the RTK/Ras pathways (Htl, Hbr and Rho) (data). The Ras signaling cascade leads to activation of the inductive transcription factor, Pnt, and inactivation of the Yan repressor. While a direct role for Mad in regulating Tin expression has been demonstrated (solid arrow; Xu et al., 1998), Wg regulation of Tin, Twi, Htl, Hbr and Rho may be either direct or indirect (dashed arrows). Additional effects of Dpp on the proximal RTK factors (our unpublished observations) are not illustrated. The five transcriptional activators assemble at and are integrated by the MHE (data) where they function synergistically (data) to promote eve expression. Specificity of the response to inductive RTK/Ras signaling derives from the combinatorial effects of the tissue-restricted and signal-activated transcription factors that converge at the MHE. In the absence of inductive signaling, Yan would repress eve by binding to the Ets sites. Since eve is a muscle and heart identity gene, the illustrated regulatory mechanisms are inferred to have a more general function in determining progenitor fates.
From Halfon et al., Cell 103:63-74 (2000).
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