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Co-ordinated control of the Aurora B abscission checkpoint by PKCε complex assembly, midbody recruitment and retention

A requirement for PKCε in exiting from the Aurora B dependent abscission checkpoint is associated with events at the midbody, however, the recruitment, retention and action of PKCε in this compartment are poorly understood. Here, the prerequisite for 14-3-3 complex assembly in this pathway is direct...

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Autores principales: Watson, Lisa, Soliman, Tanya N., Davis, Khalil, Kelly, Joanna, Lockwood, Nicola, Yang, Xiaoping, Lynham, Steven, Scott, John D., Crossland, Victoria, McDonald, Neil Q., Mann, David J., Armstrong, Alan, Eggert, Ulrike, Parker, Peter J.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8238520/
https://www.ncbi.nlm.nih.gov/pubmed/34143863
http://dx.doi.org/10.1042/BCJ20210283
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author Watson, Lisa
Soliman, Tanya N.
Davis, Khalil
Kelly, Joanna
Lockwood, Nicola
Yang, Xiaoping
Lynham, Steven
Scott, John D.
Crossland, Victoria
McDonald, Neil Q.
Mann, David J.
Armstrong, Alan
Eggert, Ulrike
Parker, Peter J.
author_facet Watson, Lisa
Soliman, Tanya N.
Davis, Khalil
Kelly, Joanna
Lockwood, Nicola
Yang, Xiaoping
Lynham, Steven
Scott, John D.
Crossland, Victoria
McDonald, Neil Q.
Mann, David J.
Armstrong, Alan
Eggert, Ulrike
Parker, Peter J.
author_sort Watson, Lisa
collection PubMed
description A requirement for PKCε in exiting from the Aurora B dependent abscission checkpoint is associated with events at the midbody, however, the recruitment, retention and action of PKCε in this compartment are poorly understood. Here, the prerequisite for 14-3-3 complex assembly in this pathway is directly linked to the phosphorylation of Aurora B S227 at the midbody. However, while essential for PKCε control of Aurora B, 14-3-3 association is shown to be unnecessary for the activity-dependent enrichment of PKCε at the midbody. This localisation is demonstrated to be an autonomous property of the inactive PKCε D532N mutant, consistent with activity-dependent dissociation. The C1A and C1B domains are necessary for this localisation, while the C2 domain and inter-C1 domain (IC1D) are necessary for retention at the midbody. Furthermore, it is shown that while the IC1D mutant retains 14-3-3 complex proficiency, it does not support Aurora B phosphorylation, nor rescues division failure observed with knockdown of endogenous PKCε. It is concluded that the concerted action of multiple independent events facilitates PKCε phosphorylation of Aurora B at the midbody to control exit from the abscission checkpoint.
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spelling pubmed-82385202021-07-08 Co-ordinated control of the Aurora B abscission checkpoint by PKCε complex assembly, midbody recruitment and retention Watson, Lisa Soliman, Tanya N. Davis, Khalil Kelly, Joanna Lockwood, Nicola Yang, Xiaoping Lynham, Steven Scott, John D. Crossland, Victoria McDonald, Neil Q. Mann, David J. Armstrong, Alan Eggert, Ulrike Parker, Peter J. Biochem J Cell Cycle, Growth & Proliferation A requirement for PKCε in exiting from the Aurora B dependent abscission checkpoint is associated with events at the midbody, however, the recruitment, retention and action of PKCε in this compartment are poorly understood. Here, the prerequisite for 14-3-3 complex assembly in this pathway is directly linked to the phosphorylation of Aurora B S227 at the midbody. However, while essential for PKCε control of Aurora B, 14-3-3 association is shown to be unnecessary for the activity-dependent enrichment of PKCε at the midbody. This localisation is demonstrated to be an autonomous property of the inactive PKCε D532N mutant, consistent with activity-dependent dissociation. The C1A and C1B domains are necessary for this localisation, while the C2 domain and inter-C1 domain (IC1D) are necessary for retention at the midbody. Furthermore, it is shown that while the IC1D mutant retains 14-3-3 complex proficiency, it does not support Aurora B phosphorylation, nor rescues division failure observed with knockdown of endogenous PKCε. It is concluded that the concerted action of multiple independent events facilitates PKCε phosphorylation of Aurora B at the midbody to control exit from the abscission checkpoint. Portland Press Ltd. 2021-06-25 2021-06-18 /pmc/articles/PMC8238520/ /pubmed/34143863 http://dx.doi.org/10.1042/BCJ20210283 Text en © 2021 The Author(s) https://creativecommons.org/licenses/by/4.0/This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and distributed under the Creative Commons Attribution License 4.0 (CC BY) (https://creativecommons.org/licenses/by/4.0/) . Open access for this article was enabled by the participation of The Francis Crick Institute in an all-inclusive Read & Publish pilot with Portland Press and the Biochemical Society under a transformative agreement with JISC.
spellingShingle Cell Cycle, Growth & Proliferation
Watson, Lisa
Soliman, Tanya N.
Davis, Khalil
Kelly, Joanna
Lockwood, Nicola
Yang, Xiaoping
Lynham, Steven
Scott, John D.
Crossland, Victoria
McDonald, Neil Q.
Mann, David J.
Armstrong, Alan
Eggert, Ulrike
Parker, Peter J.
Co-ordinated control of the Aurora B abscission checkpoint by PKCε complex assembly, midbody recruitment and retention
title Co-ordinated control of the Aurora B abscission checkpoint by PKCε complex assembly, midbody recruitment and retention
title_full Co-ordinated control of the Aurora B abscission checkpoint by PKCε complex assembly, midbody recruitment and retention
title_fullStr Co-ordinated control of the Aurora B abscission checkpoint by PKCε complex assembly, midbody recruitment and retention
title_full_unstemmed Co-ordinated control of the Aurora B abscission checkpoint by PKCε complex assembly, midbody recruitment and retention
title_short Co-ordinated control of the Aurora B abscission checkpoint by PKCε complex assembly, midbody recruitment and retention
title_sort co-ordinated control of the aurora b abscission checkpoint by pkcε complex assembly, midbody recruitment and retention
topic Cell Cycle, Growth & Proliferation
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8238520/
https://www.ncbi.nlm.nih.gov/pubmed/34143863
http://dx.doi.org/10.1042/BCJ20210283
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