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First published online 17 July 2006
doi: 10.1242/jcs.03051

Journal of Cell Science 119, 3227-3237 (2006)
Published by The Company of Biologists 2006
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Research Article

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

Andrei P. Smertenko1,*, Hsin-Yu Chang1,*, Seiji Sonobe2, Stepan I. Fenyk1, Magdalena Weingartner3, Laci Bögre3 and Patrick J. Hussey1,{ddagger}

1 The Integrative Cell Biology Laboratory, School of Biological and Biomedical Sciences, University of Durham, South Road, Durham, DH1 3LE, UK
2 Himeji Institute of Technology, Faculty of Science, Hyogo, Japan
3 School of Biological and Biomedical Sciences, Royal Holloway, University of London, Egham, TW20 0EX, UK

{ddagger} Author for correspondence (e-mail: p.j.hussey{at}durham.ac.uk)

Accepted 17 May 2006

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.

Key words: Microtubule-associated protein, MAP-65, Division midzone, Regulation




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