Control of the AtMAP65-1 interaction with microtubules through the cell cycle

Andrei P Smertenko; Hsin-Yu Chang; Seiji Sonobe; Stepan I Fenyk; Magdalena Weingartner; Laci Bögre; Patrick J Hussey

doi:10.1242/jcs.03051

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Control of the AtMAP65-1 interaction with microtubules through the cell cycle

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Control of the AtMAP65-1 interaction with microtubules through the cell cycle

Andrei P Smertenko, Hsin-Yu Chang, Seiji Sonobe, Stepan I Fenyk, Magdalena Weingartner, Laci Bögre and Patrick J Hussey

Journal of cell science, Vol.119(Pt 15), pp.3227-3237

08/01/2006

DOI: https://doi.org/10.1242/jcs.03051

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https://hdl.handle.net/2376/104017

PMID: 16847052

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Abstract

Arabidopsis Proteins - genetics

Peptide Fragments - metabolism

Phosphorylation

Cyclin-Dependent Kinases - metabolism

Fluorescence Recovery After Photobleaching

Microtubule-Associated Proteins - genetics

Microtubule-Associated Proteins - metabolism

Arabidopsis - cytology

Cells, Cultured

Recombinant Fusion Proteins - metabolism

Arabidopsis - metabolism

Tobacco - cytology

Arabidopsis Proteins - metabolism

Microtubules - metabolism

Spindle Apparatus - metabolism

Microtubules - ultrastructure

Cell Cycle - physiology

Recombinant Fusion Proteins - genetics

Signal Transduction - physiology

Peptide Fragments - genetics

Mitogen-Activated Protein Kinases - metabolism

Cell division depends on the fine control of both microtubule dynamics and microtubule organisation. The microtubule bundling protein MAP65 is a ;midzone MAP' essential for the integrity of the anaphase spindle and cell division. Arabidopsis thaliana MAP65-1 (AtMAP65-1) binds and bundles microtubules by forming 25 nm cross-bridges. Moreover, as AtMAP65-1 bundles microtubules in interphase, anaphase and telophase but does not bind microtubules in prophase or metaphase, its activity through the cell cycle must be under tight control. Here we show that AtMAP65-1 is hyperphosphorylated during prometaphase and metaphase and that CDK and MAPK are involved in this phosphorylation. This phosphorylation inhibits AtMAP65-1 activity. Expression of non-phosphorylatable AtMAP65-1 has a negative effect on mitotic progression resulting in excessive accumulation of microtubules in the metaphase spindle midzone causing a delay in mitosis. We conclude that normal metaphase spindle organisation and the transition to anaphase is dependent on inactivation of AtMAP65-1.

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Title: Control of the AtMAP65-1 interaction with microtubules through the cell cycle
Creators: Andrei P Smertenko - The Integrative Cell Biology Laboratory, School of Biological and Biomedical Sciences, University of Durham, South Road, Durham, DH1 3LE, UK
Hsin-Yu Chang
Seiji Sonobe
Stepan I Fenyk
Magdalena Weingartner
Laci Bögre
Patrick J Hussey
Publication Details: Journal of cell science, Vol.119(Pt 15), pp.3227-3237
Academic Unit: Biological Chemistry, Institute of
Publisher: England
Grant note: C18199 / Biotechnology and Biological Sciences Research Council
Identifiers: 99900546998901842
Language: English
Resource Type: Journal article