Research

We defined distinct cellular processes that independently control elongation and diametric expansion of the tracheae, thus providing a paradigm to dissect the control of tube dimensions at the cellular level. We showed that the tyrosine kinase Src42A is necessary and sufficient for polarized cell shape changes that drive tracheal tube elongation, while diametric tube expansion is controlled independently of Src42A by apical secretion. Based on this work we aim to derive a quantitative model that describes the relative contributions of distinct cellular behaviors (cell growth, cell rearrangements, and cell shape changes) and of mechanical forces in tube morphogenesis. 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 to monitor changes in cell surface area, volume, and shape over time in wild-type and in mutant situations. In collaboration with the group of PD Dr. Christof Aegerter (Physics Institute, University of Zurich), we aim to measure and manipulate mechanical forces during tube morphogenesis to experimentally test predictions derived from theoretical models.