Document Type

Theses, Masters

Master Thesis

Master thesis


Available under a Creative Commons Attribution Non-Commercial Share Alike 4.0 International Licence



Publication Details

Successfully submitted for the award of Master of Philosopy to the Technological University Dublin in


Through the use of developmental and knock out studies Mig-6 has been shown to have a role in development. It has also been shown to be a tumour suppressor gene. Little work has been done as yet looking at its role in the adult. This study examined the role of Mig-6 in the lung with the ultimate goal being to determine if the pulmonary phenotype due to Mig-6 ablation is due to a developmental programming or loss of function in the adult. This was investigated in two ways. 1. To investigate if knocking out Mig-6 in adult lung has an effect on lung function
2. Investigate the role of Mig-6 in lung epithelial cells by RNAi (Investigation of the Role of Mig-6 in Pulmonary Epithelial Cells and Vascular Cells In Vitro).
Knocking out Mig-6 in the adult mice showed no difference in epithelial markers and after staining morphology and airway size were found to be normal. This would seem to indicate that the Mig-6 phenotype is due to altered development of the lungs during the neonatal period and not due to a loss of function in the adult. From the cell work we observed differences in the effect on epithelial cells vs. endothelial
cells when Mig-6 was knocked out. The epithelial cells showed an increased number of viable cells present after knocking out Mig-6 while the number of viable cells was decreased in the endothelial cells. This would indicate that knocking out Mig-6 in epithelial cells causes increased proliferation but in endothelial cells causes apoptosis. Conclusions: Ablation of Mig-6 leads to increased proliferation in epithelial cells (and
apoptosis in endothelial cells) but knocking it out in the adult stage has a mild effect on lung




Document Type

Master thesis