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Arrested cells are Mad as Hec

Arrested cells are Mad as Hec <h2>Arrested cells are Mad as Hec</h2> Cells without Hec1 (right) stall in mitosis although Mad is not at kinetochores. Nigg/AAAS The spindle checkpoint works even when on the move, according to new results from Silvia Martin-Lluesma, Volker Stucke, and Erich Nigg (Max-Planck Institute of Biochemistry, Martinsried, Germany). Against all that has been sacred in the field, these researchers find that mitosis can be arrested when checkpoint proteins leave the kinetochore. The checkpoint is activated by Mad1 and Mad2 proteins, which bind to kinetochores that are not attached to the spindle microtubules. The prevailing theory has been that release of Mad1/Mad2 inactivates the checkpoint and allows mitosis to proceed. Nigg and colleagues looked for human Mad1-interacting proteins and found Hec1, which recruited Mad1 and Mad2 to kinetochores. Given this function, the group was surprised to find that reducing Hec1 prevented cells from dividing, despite the fact that Mad1/Mad2 were not on the kinetochores. “This is different from all that has been shown so far,” says Stucke. “The components are depleted [from kinetochores], but you still get arrest and an active checkpoint.” Hec1-depleted cells that also lacked Mad2 continued through mitosis and ended in mitotic catastrophe. Thus, checkpoint components can http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png The Journal of Cell Biology Rockefeller University Press

Arrested cells are Mad as Hec

The Journal of Cell Biology , Volume 159 (2): 201 – Oct 28, 2002

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References (1)

Publisher
Rockefeller University Press
Copyright
Copyright © 2002, by The Rockefeller University Press
ISSN
0021-9525
eISSN
1540-8140
DOI
10.1083/jcb1592rr5
Publisher site
See Article on Publisher Site

Abstract

<h2>Arrested cells are Mad as Hec</h2> Cells without Hec1 (right) stall in mitosis although Mad is not at kinetochores. Nigg/AAAS The spindle checkpoint works even when on the move, according to new results from Silvia Martin-Lluesma, Volker Stucke, and Erich Nigg (Max-Planck Institute of Biochemistry, Martinsried, Germany). Against all that has been sacred in the field, these researchers find that mitosis can be arrested when checkpoint proteins leave the kinetochore. The checkpoint is activated by Mad1 and Mad2 proteins, which bind to kinetochores that are not attached to the spindle microtubules. The prevailing theory has been that release of Mad1/Mad2 inactivates the checkpoint and allows mitosis to proceed. Nigg and colleagues looked for human Mad1-interacting proteins and found Hec1, which recruited Mad1 and Mad2 to kinetochores. Given this function, the group was surprised to find that reducing Hec1 prevented cells from dividing, despite the fact that Mad1/Mad2 were not on the kinetochores. “This is different from all that has been shown so far,” says Stucke. “The components are depleted [from kinetochores], but you still get arrest and an active checkpoint.” Hec1-depleted cells that also lacked Mad2 continued through mitosis and ended in mitotic catastrophe. Thus, checkpoint components can

Journal

The Journal of Cell BiologyRockefeller University Press

Published: Oct 28, 2002

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