Please use this identifier to cite or link to this item: https://doi.org/10.1038/s41467-018-03422-6
Title: CoA synthase regulates mitotic fidelity via CBP-mediated acetylation
Authors: Lin, C.-C
Kitagawa, M 
Tang, X
Hou, M.-H
Wu, J
Qu, D.C
Srinivas, V 
Liu, X
Thompson, J.W
Mathey-Prevot, B
Yao, T.-P
Lee, S.H 
Chi, J.-T
Keywords: acyltransferase
alpha tubulin
aurora A kinase
beta tubulin
coenzyme A
coenzyme A synthase
cyclic AMP responsive element binding protein binding protein
cyclin B1
cycloheximide
enzyme
messenger RNA
protein
top2a protein
tpx2 protein
unclassified drug
aurora A kinase
cell cycle protein
COASY protein, human
cyclic AMP responsive element binding protein binding protein
microtubule associated protein
nuclear protein
protein binding
TPX2 protein, human
transferase
chemical analysis
chemical reaction
enzyme
enzyme activity
molecular analysis
protein
acetylation
Article
cancer cell culture
controlled study
cytokinesis
enzyme activation
enzyme activity
gene inactivation
genomic instability
human
human cell
in vitro study
interphase
mitosis
protein degradation
protein stability
triple negative breast cancer
ubiquitination
acetylation
cell line
genetics
metabolism
Acetylation
Aurora Kinase A
Cell Cycle Proteins
Cell Line
CREB-Binding Protein
Humans
Microtubule-Associated Proteins
Mitosis
Nuclear Proteins
Protein Binding
Transferases
Issue Date: 2018
Publisher: Nature Publishing Group
Citation: Lin, C.-C, Kitagawa, M, Tang, X, Hou, M.-H, Wu, J, Qu, D.C, Srinivas, V, Liu, X, Thompson, J.W, Mathey-Prevot, B, Yao, T.-P, Lee, S.H, Chi, J.-T (2018). CoA synthase regulates mitotic fidelity via CBP-mediated acetylation. Nature Communications 9 (1) : 1039. ScholarBank@NUS Repository. https://doi.org/10.1038/s41467-018-03422-6
Abstract: The temporal activation of kinases and timely ubiquitin-mediated degradation is central to faithful mitosis. Here we present evidence that acetylation controlled by Coenzyme A synthase (COASY) and acetyltransferase CBP constitutes a novel mechanism that ensures faithful mitosis. We found that COASY knockdown triggers prolonged mitosis and multinucleation. Acetylome analysis reveals that COASY inactivation leads to hyper-acetylation of proteins associated with mitosis, including CBP and an Aurora A kinase activator, TPX2. During early mitosis, a transient CBP-mediated TPX2 acetylation is associated with TPX2 accumulation and Aurora A activation. The recruitment of COASY inhibits CBP-mediated TPX2 acetylation, promoting TPX2 degradation for mitotic exit. Consistently, we detected a stage-specific COASY-CBP-TPX2 association during mitosis. Remarkably, pharmacological and genetic inactivation of CBP effectively rescued the mitotic defects caused by COASY knockdown. Together, our findings uncover a novel mitotic regulation wherein COASY and CBP coordinate an acetylation network to enforce productive mitosis. © 2018 The Author(s).
Source Title: Nature Communications
URI: https://scholarbank.nus.edu.sg/handle/10635/174236
ISSN: 2041-1723
DOI: 10.1038/s41467-018-03422-6
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