Abstract
ABSTRACTThe Drosophila embryonic tracheal network is an excellent model to study tube size. The chitin-based apical luminal matrix and cell polarity are well known to regulate tube size in Drosophila trachea. Defects in luminal matrix and cell polarity lead to tube overexpansion. Here, we address the novel function of the rebuff (reb) gene, which encodes an evolutionarily conserved Smad-like protein. In reb mutants, tracheal tubes are moderately over-elongated. Despite the establishment of normal cell polarity, we observed significantly reduced apical luminal matrix in reb mutants. Among various luminal components, luminal Obstructor-A (ObstA) is drastically reduced. Interestingly, ObstA is localized in vesicle-like structures that are apically concentrated in reb mutants. To investigate the possibility that reb is involved in the endocytosis of ObstA, we analyzed the co-localization of ObstA and endocytic markers in reb mutants. We observed that ObstA is localized in late endosomes and recycling endosomes. This suggests that in reb mutant trachea, endocytosed ObstA is degraded or recycled back to the apical region. However, ObstA vesicles are retained in the apical region and are failed to be secreted to the lumen. Taken together, these results suggest one function of reb is regulating the endocytosis of luminal matrix components.
Highlights
Distinct tube size is critical for the function of human tubular organs such as the lung, vascular system and kidney
The specification of tracheal tubes depends on signaling pathways, such as epithelial growth factor (EGF) and transforming growth factor (TGF-β) signaling, that are activated in a given group of cells (Llimargas and Casanova, 1999; Chen et al, 1998; Chihara and Hayashi, 2000)
We observed co-localization of ObstA and Rab7, ObstA and Rab11 and ObstA and Vps26. These results suggest that in reb mutant trachea, internalized ObstA could be degraded in lysosomes mediated by Rab7, or be recycled back to the apical region mediated by Rab11 and retromer
Summary
Distinct tube size is critical for the function of human tubular organs such as the lung, vascular system and kidney. Aberrant tube sizes lead to devastating human illnesses such as ischemic tissue injury and polycystic kidney disease. Studies in Drosophila trachea have shed light on mechanisms of tube-size regulation. The Drosophila trachea is the major airway consisting of branches with well-defined and consistent dimensions. Tracheal branches are formed by single layers of epithelial cells with the apical surface facing the luminal matrix and basal surface facing the surrounding tissues. The specification of tracheal tubes depends on signaling pathways, such as epithelial growth factor (EGF) and transforming growth factor (TGF-β) signaling, that are activated in a given group of cells (Llimargas and Casanova, 1999; Chen et al, 1998; Chihara and Hayashi, 2000).
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