Please find open theses positions below.

In addition, we are always happy to receive unsolicited applications from committed and motivated students with an interest in (translational) basic science.

Master Thesis

The group of Prof. Frick is seeking motivated students to work on

Controlling airway mucus secretion


Background: Airway mucus forms an essential barrier that protects the lungs from inhaled particles, pathogens and chemicals. These toxicants are entrapped in mucus, then swept out of the lungs by ciliary action. However, high levels of mucin production coupled with rapid secretion can lead to occlusion of the airways by mucus. This contributes to airflow obstruction, inflammation, and infection in multiple lung diseases, including asthma, chronic obstructive pulmonary disease (COPD), and cystic fibrosis.

Mucins, the principal macromolecular components of mucus, are secreted via exocytosis from secretory cells within the airway epithelium. They are secreted both at a low baseline rate, and a high stimulated rate thousands-fold greater than baseline (often upon exposure to allergens, parasites, or viruses.) However, the detailed molecular mechanisms that regulate baseline and stimulated secretion are incompletely understood.

Within our group we aim to 1) identify the detailed molecular mechanisms that regulate exocytosis of mucin containing vesicles in secretory airway cells (see Hoang et al., Am J Respir Crit Care Med. 2022), and 2) exploit these to develop novel therapeutics that selectively inhibit “excessive” stimulated mucin secretion without impairing homeostatic baseline secretion (see Lai et al. Nature. 2022, Dickey et al. Clin Transl Med., 2022).


We have recently developed a small peptide-based inhibitor (SP9) that selectively blocks stimulated mucin secretion without impairing homeostatic baseline secretion (Lai et al. Nature. 2022). SP9 requires conjugation to cell penetrating peptides for delivery into the cytosol of the secretory airway cells. The aim of the thesis project is to investigate the detailed cellular mechanism of SP9 uptake into the cytosol of target cells


  • Cell culture of primary airway epithelial cells and cell lines
  • Pharmacological and genetic modification of cellular internalization pathways
  • (Quantitative) Analysis of peptide internalization into target cells (Immunofluorescence microscopy, FACS)
  • Data analysis, interpretation

If you are interested in joining a friendly, interdisciplinary and multicultural team please contact manfred.frick(at)

The group of Prof. Frick is seeking motivated students to work on

Epithelial – Fibroblast crosstalk in the onset of Idiopathic Pulmonary Fibrosis (IPF)


Background: Idiopathic pulmonary fibrosis (IPF) is a fatal respiratory disease characterized by aberrant fibroblast activation and progressive fibrotic remodelling of the lungs. The exact pathophysiological mechanisms of IPF remain unknown. The current conceptual model for the pathogenesis of IPF suggests that 1) recurrent micro-injuries to the bronchoalveolar epithelium initiate abnormal repair and wound healing responses in the lung. Damaged epithelial cells secrete pro-fibrotic mediators that activate alveolar fibroblasts. Activated fibroblasts proliferate, differentiate into highly active myofibroblasts and deposit excessive amounts of extracellular matrix (ECM). This results in fibrotic tissue remodeling with increased tissue stiffness. 2) Fibroblasts sense and respond to the increased rigidity of the ECM. This perpetuates the fibrotic response in a progressive feed-forward loop between increasing matrix stiffness, myofibroblast activation and expression and cross-linking of ECM proteins, which eventually leads to respiratory insufficiency and death.

Within our group we aim to identify mechanisms that 1) trigger the onset of disease (i.e. pro-fibrotic factors released from epithelial cells), and 2) drive progressive fibroblast activation



The aim of the thesis project is to establish alveolar epithelial damage models in vitro and to test the pro-fibrotic potential of the epithelial cell supernatants for activation of primary lung fibroblasts.



  • Cell culture of primary lung epithelial cells and fibroblasts
  • Use of biomechanical cell culture models (e.g. cell stretching)
  • Analysis of fibroblast activation (RT-PCR, Western Blot, Immunofluoresence)
  • Sample preparation for MassSpec analysis
  • Data analysis, interpretation


If you are interested in joining a friendly, interdisciplinary and multicultural team please contact manfred.frick(at)

The group of PD Dr. Felder is seeking a student

Mechanosensing by stretch-induced unfolding of desmoplakin


Background: Cells of various tissues are exposed to mechanical stress that trigger specific cellular effects or protective mechanisms. Although such responses may vary in speed, the activated signaling cascade and other parameters, they all depend on a mechanically altered molecular sensor to initiate the desired effect. Only few of these sensor molecules (mostly proteins) are known and the response mechanisms on a molecular level – like deformation or unfolding – are far from being entirely understood.

Desmosomes (D) are tension-resistant cell junctions where intermediate filaments (IF) insert and connect the IF-networks of adjacent cells. We found that the altered ultrastructure of D in stretched cells could be well explained by an unfolding of desmoplakin - an important protein in D. Since mathematical simulations not only show that extension of desmoplakin unfolds the protein but also exposes an SH-binding site (Daday et al ‘17) we hypothesize that our findings might be one of the few cases where a mechanosensor is shown “at work”.


Since our hypothesis is predominantly based on morphological observations, functional assays need to confirm desmoplakin’s role as a stretch-induced mechanosensor.    



  • Cell culture of cell lines under conventional culture conditions and on elastic silicone membranes that are used for cell stretching
  • Assays (commercially available mol-biol kits) to prove a conformational change of desmoplakin upon stretch
  • Modification/elimination of desmoplakin’s SH-domain to abolish a mechanically induced mechanosensation by desmoplakin   
  • Immunofluorescence and electron microscopy if required


If you are interested please contact edward.felder(at)

PhD Thesis

The group of Prof. Frick is looking for a talented and highly motivated PhD candidate (m/f/d) with an interest in cell biology, molecular biology, biochemistry, and respiratory physiology. We welcome applications from candidates with a recent MSc-degree in life sciences for the PhD project: Molecular mechanisms of airway mucin secretion.

For details see: