Abstracts of papers presented at the 25th Genetics Societys Mammalian Genetics and Development Workshop held at the Institute of Child Health University College London on 7th November 2014.

摘要

During neurulation, the neural plate bends around the median hinge point (MHP), overlying the notochord. MHP cells spend more time in G1/S-phase of the cell cycle than lateral cells, and this is associated with adoption of a wedged cell shape due to interruption of interkinetic nuclear migration. Clustering of wedge shaped cells in the MHP drives midline bending. To determine the mechanism underlying the prolonged cell cycle in the MHP, we examined the expression of cell cycle inhibitors, and found the cyclin-dependent kinase inhibitors (CDKIs), p21 and p57, expressed in midline cells. p21 null mice, which exhibit median hinge point formation, show upregulation of p57 in midline cells, supporting our hypothesis of a redundant relationship between p21 and p57 during neural plate bending. Detailed cell cycle analysis in vivo and in vitro is being undertaken to examine if loss of cyclin-dependent kinase inhibitors, by genetic ablation and electroporation, leads to shortening of G1/S-phase in cells of the median hinge point, thereby disrupting cell wedging and neural plate bending.