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.