Compared to lung development also kidney ureters develops by first forming an ureteral bud followed by branching morphogenesis. Like in the lung tracheal budding ZO-1 is required in ureter bud formation of rat tissues [28] . Branching morphogenesis is promoted by ezrin which is activated by growth factors EGF (Epidermal growth factor), HGF (Hepatic growth factor) or interleukin-1alpha by tyrosine phosphorylation. MT-MMP1 (Membrane type matrix metalloproteinase 1) and MMP2 (Matrix metalloproteinase 2) are secreted on tips of the epithelial branches and proliferation is higher in epithelial cells in those areas [28] . Proteins of adherence junctions such as E-cadherin, are expressed a bit Mesothelial cells 1,2, 3,5,7 [104, 107] earlier, however there is a gradual increase of claudin 3 and ZO-1 from day 3 to 5 in cultured ureteric buds [28] . Anatomically, the branching morphogenesis in the lung differs from the ureteric development in that in the ureteral development there is no lateral branching [28] . Also EGF (Epidermal growth factor) seems to be important for lung organogenesis, deletion of EGFR (Epidermal growth factor receptor) leads to impaired branching and deficient alveolisation, and pneumocytes remain immature [34] . Prealveolar fetal alveolar lung cells express claudin-1, 3, 4, 5, 7, 9, 10 and 18 mRNAs [16] . mRNAs for occludin, JAM-1, ZO-1, ZO-2, and ZO-3 are also present [16] . In experimental models on alveolar cell differentiation undifferentiated fetal alveolar epithelial cells increase their transepithelial resistance under the influence of cell culture medium containing dexamethasone, 8-bromo-cAMP and isobuthylmethylxanthanine and transform to type 2 alveolar cells at the same time increasing the claudin 5 and 18 mRNA levels and decreasing claudin 1 mRNA [16] . On the other hand, EGF stimulated fetal alveolar type 2 cells show a decrease in claudin 5 and 3 mRNA but an increase in claudins 4 and 7 mRNA while increasing their transepithelial resistance and transforming to type 1 cells [25] . While such in vitro models may differ from physiological conditions, changes in claudin expression apparently modulate or follow phenotypic changes in lung bronchial or alveolar cells during organogenesis. Such studies also emphasize EGF's role in lung alveolar development.