Anchor negatively regulates BMP signaling to control Drosophila wing development

ABSTRACT Summary statement The novel gene anchor is the ortholog of vertebrate GPR155, which contributes to preventing wing disc tissue overgrowth and limiting the phosphorylation of Mad in presumptive veins during the pupal stage. G protein-coupled receptors play a particularly important function in many organisms. The novel Drosophila gene anchor is the ortholog of vertebrate GPR155, and its molecular function and biological process are not yet known, especially in wing development. Knocking down anchor resulted in increased wing size and extra and thickened veins. These abnormal wing phenotypes are similar to those observed in gain-of-function of BMP signaling experiments. We observed that the BMP signaling indicator p-Mad was significantly increased in anchor RNAi-induced wing discs in larvae and that it also abnormally accumulated in intervein regions in pupae. Furthermore, the expression of BMP signaling pathway target genes were examined using a lacZ reporter, and the results indicated that omb and sal were substantially increased in anchor knockdown wing discs. In a study of genetic interactions between Anchor and BMP signaling pathway, the broadened and ectopic vein tissues were rescued by knocking down BMP levels. The results suggested that the function of Anchor is to negatively regulate BMP signaling during wing development and vein formation, and that Anchor targets or works upstream of Dpp.