|Title||RTK signaling modulates the Dorsal gradient.|
|Publication Type||Journal Article|
|Year of Publication||2012|
|Authors||Helman, A, Lim, B, Andreu, MJosé, Kim, Y, Shestkin, T, Lu, H, Jiménez, G, Shvartsman, SY, Paroush, Z'ev|
|Date Published||2012 Aug|
|Keywords||Animals, Animals, Genetically Modified, Basic Helix-Loop-Helix Transcription Factors, Body Patterning, Drosophila melanogaster, Drosophila Proteins, Feedback, Physiological, Gene Expression Regulation, Developmental, Genes, Insect, HMGB Proteins, Intracellular Signaling Peptides and Proteins, Models, Biological, Mutation, Nuclear Proteins, Phosphoproteins, Receptor Protein-Tyrosine Kinases, Receptor, Epidermal Growth Factor, Receptors, Invertebrate Peptide, Repressor Proteins, Signal Transduction, Transcription Factors|
The dorsoventral (DV) axis of the Drosophila embryo is patterned by a nuclear gradient of the Rel family transcription factor, Dorsal (Dl), that activates or represses numerous target genes in a region-specific manner. Here, we demonstrate that signaling by receptor tyrosine kinases (RTK) reduces nuclear levels and transcriptional activity of Dl, both at the poles and in the mid-body of the embryo. These effects depend on wntD, which encodes a Dl antagonist belonging to the Wingless/Wnt family of secreted factors. Specifically, we show that, via relief of Groucho- and Capicua-mediated repression, the Torso and EGFR RTK pathways induce expression of WntD, which in turn limits Dl nuclear localization at the poles and along the DV axis. Furthermore, this RTK-dependent control of Dl is important for restricting expression of its targets in both contexts. Thus, our results reveal a new mechanism of crosstalk, whereby RTK signals modulate the spatial distribution and activity of a developmental morphogen in vivo.