The seven-pass transmembrane cadherin Flamingo controls dendritic self-avoidance via its binding to a LIM domain protein, Espinas, in Drosophila sensory neurons

Members of the Flamingo cadherin family are required in a number of different in vivo contexts of neural development, including growth control of dendrites, axonal navigation, tract formation, and target selection. The authors demonstrate that Esn binds to the carboxyl cytoplasmic tail (C-tail) of Fmi and that this binding was critical for dendritic self-avoidance

A novel planar polarity genepepsinogen-likeregulateswinglessexpression in a posttranscriptional manner

Background: Planar cell polarity (PCP) originally referred to the coordination of global organ axes and individual cell polarity within the plane of the epithelium. More recently, it has been accepted that pertinent PCP regulators play essential roles not only in epithelial sheets, but also in various rearranging cells. Results: We identified pepsinogen-like (pcl) as a new planar polarity gene, using Drosophila wing epidermis as a model. Pcl protein is predicted to belong to a family of aspartic proteases. When pcl mutant clones were observed in pupal wings, PCP was disturbed in both mutant and wild-type cells that were juxtaposed to the clone border. We examined levels of known PCP proteins in wing imaginal discs. The amount of the seven-pass transmembrane cadherin Flamingo (Fmi), one of the PCP “core group” members, was significantly decreased in mutant clones, whereas neither the amount of nor the polarized localization of Dachsous (Ds) at cell boundaries was affected. In addition to the PCP phenotype, the pcl mutation caused loss of wing margins. Intriguingly, this was most likely due to a dramatic decrease in the level of Wingless (Wg) protein, but not due to a decrease in the level of wg transcripts. Conclusions: Our results raise the possibility that Pcl regulates Wg expression post-transcriptionally, and PCP, by proteolytic cleavages