dc.contributor.author | Pike, T | en_US |
dc.contributor.author | Brownlow, N | en_US |
dc.contributor.author | Kjaer, S | en_US |
dc.contributor.author | Carlton, J | en_US |
dc.contributor.author | Parker, PJ | en_US |
dc.date.accessioned | 2020-10-12T10:48:35Z | |
dc.date.available | 2016-11-03 | en_US |
dc.date.issued | 2016-12-22 | en_US |
dc.identifier.uri | https://qmro.qmul.ac.uk/xmlui/handle/123456789/67504 | |
dc.description.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. | en_US |
dc.format.extent | 13853 - ? | en_US |
dc.language | eng | en_US |
dc.relation.ispartof | Nat Commun | en_US |
dc.rights | Attribution 3.0 United States | * |
dc.rights.uri | http://creativecommons.org/licenses/by/3.0/us/ | * |
dc.subject | Amino Acid Sequence | en_US |
dc.subject | Anaphase | en_US |
dc.subject | Aurora Kinase B | en_US |
dc.subject | Cell Cycle Checkpoints | en_US |
dc.subject | Cell Cycle Proteins | en_US |
dc.subject | Cell Line | en_US |
dc.subject | Cytokinesis | en_US |
dc.subject | Endosomal Sorting Complexes Required for Transport | en_US |
dc.subject | HEK293 Cells | en_US |
dc.subject | Humans | en_US |
dc.subject | Models, Biological | en_US |
dc.subject | Mutation | en_US |
dc.subject | Phosphorylation | en_US |
dc.subject | Protein Kinase C-epsilon | en_US |
dc.subject | Recombinant Proteins | en_US |
dc.subject | Signal Transduction | en_US |
dc.subject | Substrate Specificity | en_US |
dc.title | PKCɛ switches Aurora B specificity to exit the abscission checkpoint. | en_US |
dc.type | Article | |
dc.identifier.doi | 10.1038/ncomms13853 | en_US |
pubs.author-url | https://www.ncbi.nlm.nih.gov/pubmed/28004745 | en_US |
pubs.notes | Not known | en_US |
pubs.publication-status | Published online | en_US |
pubs.volume | 7 | en_US |
dcterms.dateAccepted | 2016-11-03 | en_US |