A cancer-associated, genome protective programme engaging PKCε.

Associated with their roles as targets for tumour promoters, there has been a long-standing interest in how members of the protein kinase C (PKC) family act to modulate cell growth and division. This has generated a great deal of observational data, but has for the most part not afforded clear mechanistic insights into the control mechanisms at play. Here, we review the roles of PKCε in protecting transformed cells from non-disjunction.

Author Correction: The Aurora B specificity switch is required to protect from non-disjunction at the metaphase/anaphase transition.

An amendment to this paper has been published and can be accessed via a link at the top of the paper.

The Aurora B specificity switch is required to protect from non-disjunction at the metaphase/anaphase transition.

The Aurora B abscission checkpoint delays cytokinesis until resolution of DNA trapped in the cleavage furrow. This process involves PKCε phosphorylation of Aurora B S227. Assessing if this PKCε-Aurora B module provides a more widely exploited genome-protective control for the cell cycle, we show Aurora B phosphorylation at S227 by PKCε also occurs during mitosis.