Ptk7 Regulates Epididymal Duct Coiling Through Regulating Myosin Ii Activity in the Surrounding Mesenchyme Cells of the Epididymal Duct.
PTK7 Regulates Epididymal Duct Coiling Through Regulating Myosin II Activity in the Surrounding Mesenchyme Cells of the Epididymal Duct.
By
Angela Washington
Research under the supervision of Dr. Barry T. Hinton of the Department of Cell
Biology at the University of Virginia Health Systems
Summer Session III 2012
Abstract
It is very clear that the epididymis plays a crucial role in the maturation of spermatozoa and without a fully developed and functional epididymis male infertility will result. We are especially interested in understanding the mechanisms that regulate the development of this important organ because disruptions to epididymal function will also arise as a consequence of abnormal development. Very little is known either of the process of epididymal development or the nature and causes of congenital defects that lead to male infertility. A major event during Wolffian/epididymal duct embryonic development is elongation and coiling. It is hypothesized that elongation is the result of cell proliferation coupled with directed cell rearrangements, Coiling is regulated by the planar cell polarity signaling pathway (PCP). PTK7 is a major regulator of non-canonical PCP pathway. Our previous study discovered that mice are null for Ptk7 have a shortened epididymal duct and an unusually coiling pattern compared to wild type duct at the same age. In this study we indicated the epithelial and mesenchymal cells in the PTK7 knockout epidymides were less organized compared to the control. Although the basal to apical polarity of epithelial cells and the formation of extracellular matrix (ECM) at the base of epithelium did not impaired by PTK7 ablation, the myosin II activity was affected in the surrounding mesenchymal cells of epididymal duct after loss of PTK7 in the epididymis. In addition, at E18.5 coiling is proceeding in a proximal to distal manner, with more coiling activity in the proximal region and less activity in the distal region.
By
Angela Washington
Research under the supervision of Dr. Barry T. Hinton of the Department of Cell
Biology at the University of Virginia Health Systems
Summer Session III 2012
Abstract
It is very clear that the epididymis plays a crucial role in the maturation of spermatozoa and without a fully developed and functional epididymis male infertility will result. We are especially interested in understanding the mechanisms that regulate the development of this important organ because disruptions to epididymal function will also arise as a consequence of abnormal development. Very little is known either of the process of epididymal development or the nature and causes of congenital defects that lead to male infertility. A major event during Wolffian/epididymal duct embryonic development is elongation and coiling. It is hypothesized that elongation is the result of cell proliferation coupled with directed cell rearrangements, Coiling is regulated by the planar cell polarity signaling pathway (PCP). PTK7 is a major regulator of non-canonical PCP pathway. Our previous study discovered that mice are null for Ptk7 have a shortened epididymal duct and an unusually coiling pattern compared to wild type duct at the same age. In this study we indicated the epithelial and mesenchymal cells in the PTK7 knockout epidymides were less organized compared to the control. Although the basal to apical polarity of epithelial cells and the formation of extracellular matrix (ECM) at the base of epithelium did not impaired by PTK7 ablation, the myosin II activity was affected in the surrounding mesenchymal cells of epididymal duct after loss of PTK7 in the epididymis. In addition, at E18.5 coiling is proceeding in a proximal to distal manner, with more coiling activity in the proximal region and less activity in the distal region.