We defined distinct cellular processes that independently control tracheal tube elongation and diametric expansion. We showed that the conserved tyrosine kinase Src42 induces axially polarized cell shape changes that drive tracheal tube elongation (Förster and Luschnig 2012). Conversely, diametric tube expansion is controlled independently of Src42 by apical secretion. Secretory activity drives luminal expansion in a cell-autonomous fashion by promoting apical membrane growth and cell flattening. A cell-intrinsic program, rather than non-autonomous extrinsic cues, controls the dimensions of tracheal tubes. Our findings provide a framework to dissect the control of tube dimensions at the cellular and molecular level. We ask how cells sense and respond to mechanical forces, such as anisotropic tissue tension, which are imposed by the cylindrical geometry of tubular epithelia. To analyze cellular behavior during tracheal tube expansion, we employ genetic labeling and imaging tools. We also aim to measure and manipulate mechanical forces during tube morphogenesis to experimentally test predictions derived from theoretical models.
Cell Behavior and Mechanical Forces in Cylindrical Epithelia
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Src42A-dependent polarized cell shape changes mediate epithelial tube elongation in Drosophila
Nature Cell Biology |
| Volume: 14 | Issue: 5 | 526-34 | 
Abstract
Although many organ functions rely on epithelial tubes with correct dimensions, mechanisms underlying tube size control are poorly understood. We analyse the cellular mechanism of tracheal tube elongation in Drosophila, and describe an essential role of the conserved tyrosine kinase Src42A in this process. We show that Src42A is required for polarized cell shape changes and cell rearrangements that mediate tube elongation. In contrast, diametric expansion is controlled by apical secretion independently of Src42A. Constitutive activation of Src42A induces axial cell stretching and tracheal overelongation, indicating that Src42A acts instructively in this process. We propose that Src42A-dependent recycling of E-Cadherin at adherens junctions is limiting for cell shape changes and rearrangements in the axial dimension of the tube. Thus, we define distinct cellular processes that independently control axial and diametric expansion of a cylindrical epithelium in a developing organ. Whereas exocytosis-dependent membrane growth drives circumferential tube expansion, Src42A is required to orient membrane growth in the axial dimension of the tube.