Introduction

Earlier work on PKCε provided evidence of its role in completing cytokinesis in a subset of tumour cell models. Further analysis has demonstrated that this property is exacerbated by earlier cell cycle stress that is also influenced by PKCε action.

Some of our earlier work on PKCε provided evidence of its role in completing cytokinesis in a subset of tumour cell models. Further analysis has demonstrated that this property is related to earlier cell cycle stress that is itself influenced by PKCε action. Specifically we have shown that sister chromatid non-disjunction at the metaphase-anaphase transition triggers a PKCε dependent delay in anaphase entry.

We are employing various molecular, chemical biology, cellular and imaging approaches ex vivo and in vivo to better understand the role PKCε plays both at this metaphase-anaphase transition and at cytokinesis. Molecular analysis of the behaviour of the spindle assembly checkpoint (SAC) and the abscission checkpoint are both providing detailed insights into PKCε action. How and when these processes are engaged, and what distinguishes the normal from the transformed state, comprise additional avenues of work that will inform on possible PKCε interventions.