Mitotic activity of survivin is regulated by acetylation at K129

Survivin is a cancer-associated protein regulated by multiple factors, including acetylation at K129 within its C-terminal α-helical tail. Acetylation of survivin is being pursued as a potential prognostic marker in breast cancer. This modification at K129 may cause nuclear accumulation of survivin...

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Bibliographic Details
Published in:Cell cycle (Georgetown, Tex.) Tex.), 2015-01, Vol.14 (11), p.1738-1747
Main Authors: Aljaberi, Aysha M, Webster, Jamie Rm, Wheatley, Sally P
Format: Article
Language:English
Subjects:
Acetylation
Chromosome Segregation - genetics
Chromosome Segregation - physiology
Cytokinesis - genetics
Cytokinesis - physiology
HeLa Cells
Humans
Inhibitor of Apoptosis Proteins - metabolism
Microscopy, Fluorescence
Mitosis - genetics
Mitosis - physiology
Mutation, Missense - genetics
Time-Lapse Imaging
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Summary:Survivin is a cancer-associated protein regulated by multiple factors, including acetylation at K129 within its C-terminal α-helical tail. Acetylation of survivin is being pursued as a potential prognostic marker in breast cancer. This modification at K129 may cause nuclear accumulation of survivin in interphase cells; however, whether this affects its essential role during mitosis has not been addressed. We posited whether mimicking acetylation of survivin at K129 alters its activity during mitosis. Fluorescence microscopy and time-lapse imaging showed that, mutating this site to an alanine to act as a constitutive acetyl mimetic, K129A, causes defects in chromosome segregation and cytokinesis. As a non-acetylatable version, K129R, also has difficulty during mitotic exit, we conclude that cyclical acetylation and deacetylation is required for fully functional survivin during mitosis.
ISSN:1538-4101
1551-4005
DOI:10.1080/15384101.2015.1033597