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Pax3 induces cell aggregation and regulates phenotypic mesenchymal-epithelial interconversion.
O'Neil Wiggan1, Marc P Fadel, Paul A Hamel
1Department of Laboratory Medicine and Pathobiology, Faculty of Medicine, University of Toronto, Toronto, Ontario, M5S 1A8 Canada.
Journal of Cell Science
|February 28, 2002
Summary
Paired box 3 (Pax3) gene expression in mammalian cells triggers a switch from mesenchymal to epithelial characteristics. This novel morphogenetic activity of Pax3 is crucial for embryonic development, impacting somite and neural tube formation.
Area of Science:
- Developmental Biology
- Molecular Biology
- Cell Biology
Background:
- Paired box (Pax) transcription factors are essential for embryonic pattern formation.
- Mutations in Pax genes, like Pax3, lead to morphological defects in mammals.
- The specific cellular processes regulated by Pax genes remain largely uncharacterized.
Purpose of the Study:
- To investigate the cellular functions of Pax3.
- To elucidate the role of Pax3 in regulating cell morphology and tissue organization.
- To understand the contribution of Pax3 to embryonic development.
Main Methods:
- Ectopic expression of Pax3 in mesenchymal mammalian cell lines.
- Analysis of cell aggregation, morphology, and cytoskeletal architecture.
- Assessment of epithelial-to-mesenchymal transition (EMT) and mesenchymal-to-epithelial transition (MET) markers.
Main Results:
- Ectopic Pax3 expression induced the formation of multi-layered cell aggregates with epithelial traits.
- Pax3 altered cell size, shape, and cytoskeleton, promoting a mesenchymal-to-epithelial transition (MET).
- Pax3 also primed cells for subsequent hepatocyte growth factor/scatter factor (HGF/SF)-induced epithelial-to-mesenchymal transition (EMT).
Conclusions:
- Pax3 exhibits novel morphogenetic activity, driving MET in mammalian cells.
- Absence of Pax3 in vivo is predicted to cause developmental defects in somites and neural tube.
- Pax3 plays a critical role in regulating cellular transitions essential for embryonic development.