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Abstract
The transcription factor GATA6 is expressed in the fetal pulmonary epithelium of the
developing mouse lung and loss of function studies strongly suggested that it is required
for proper branching morphogenesis and epithelial differentiation. We have further
investigated the role of GATA6 in this process by utilizing a pulmonary epithelium
specific promoter to maintain high levels of GATA6 protein during fetal lung development.
Transgenic mice expressing Gata6 cDNA under the control of the human Surfactant Protein-C
(SP-C) promoter were generated and their lungs were analyzed during fetal stages.
Transgenic lungs exhibit branching defects as early as embryonic day (E) 14.5 and
molecular analysis just before birth (E18.5) shows a lack of distal epithelium differentiation
whereas proximal epithelium is unaffected. Electron microscopic analysis and glycogen
staining confirm the lack of differentiation to mature Type II cells. Thus, elevated
levels of GATA6 protein affect early lung development and in analogy to other GATA
factors in other tissues, GATA6 also plays a crucial role in the terminal differentiation
in this case of the distal pulmonary epithelium.