PKCɛ switches Aurora B specificity to exit the abscission checkpoint View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2016-12-22

AUTHORS

Tanya Pike, Nicola Brownlow, Svend Kjaer, Jeremy Carlton, Peter J Parker

ABSTRACT

The 'NoCut', or Aurora B abscission checkpoint can be activated if DNA is retained in the cleavage furrow after completion of anaphase. Checkpoint failure leads to incomplete abscission and a binucleate outcome. These phenotypes are also observed after loss of PKCɛ in transformed cell models. Here we show that PKCɛ directly modulates the Aurora B-dependent abscission checkpoint by phosphorylating Aurora B at S227. This phosphorylation invokes a switch in Aurora B specificity, with increased phosphorylation of a subset of target substrates, including the CPC subunit Borealin. This switch is essential for abscission checkpoint exit. Preventing the phosphorylation of Borealin leads to abscission failure, as does expression of a non-phosphorylatable Aurora B S227A mutant. Further, depletion of the ESCRT-III component and Aurora B substrate CHMP4C enables abscission, bypassing the PKCɛ-Aurora B exit pathway. Thus, we demonstrate that PKCɛ signals through Aurora B to exit the abscission checkpoint and complete cell division. More... »

PAGES

13853

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/ncomms13853

DOI

http://dx.doi.org/10.1038/ncomms13853

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1021318965

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28004745


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