Epithelial tubes are the functional units of many organs, and proper tube geometry is crucial for organ function. Here, we characterize serrano (sano), a novel cytoplasmic protein that is apically enriched in several tube-forming epithelia in Drosophila, including the tracheal system. Loss of sano results in elongated tracheae, whereas Sano overexpression causes shortened tracheae with reduced apical boundaries. Sano overexpression during larval and pupal stages causes planar cell polarity (PCP) defects in several adult tissues. In Sano-overexpressing pupal wing cells, core PCP proteins are mislocalized and prehairs are misoriented; sano loss or overexpression in the eye disrupts ommatidial polarity and rotation. Importantly, Sano binds the PCP regulator Dishevelled (Dsh), and loss or ectopic expression of many known PCP proteins in the trachea gives rise to similar defects observed with loss or gain of sano, revealing a previously unrecognized role for PCP pathway components in tube size control.
Tubular organ formation is a ubiquitous process required to sustain life in multicellular organisms. In this study, we focused on the tracheal system of the fruit fly, Drosophila melanogaster, and identified Serrano (Sano) as a novel protein expressed in several embryonic tubular organs, including trachea. sano loss results in over-elongated trachea, whereas Sano overexpression causes shortened trachea, suggesting that sano is required for proper tracheal tube length. Interestingly, Sano overexpression results in typical planar cell polarity (PCP) defects in many adult tissues and pupal wing cells. The PCP pathway is highly conserved from flies to mammals and it has been known to control cell polarity within the plane of epithelial tissues. Importantly, we found that Sano binds Dishevelled (Dsh), a key PCP regulator, and loss or ectopic expression of many known PCP proteins in the trachea give rise to similar defects observed with loss or gain of sano, suggesting a new role for the PCP genes in tube length control. Interestingly, the changes in tube length and PCP defects in the wing were linked to changes in apical domain size, suggesting that Sano and the PCP components affect either membrane recycling and/or the linkage of the membrane to the cytoskeleton.