The Functional Antagonism between Eg5 and Dynein in Spindle Bipolarization Is Not Compatible with a Simple Push-Pull Model

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Cell Reports. 2012, 1(5), pp. 408-416. ISSN 2211-1247. eISSN 2211-1247. Available under: doi: 10.1016/j.celrep.2012.03.006
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During cell division, the molecular motor Eg5 crosslinks overlapping antiparallel microtubules and pushes them apart to separate mitotic spindle poles. Dynein has been proposed as a direct antagonist of Eg5 at the spindle equator, pulling on antiparallel microtubules and favoring spindle collapse. Some of the experiments supporting this hypothesis relied on endpoint quantifications of spindle phenotypes rather than following individual cell fates over time. Here, we present a mathematical model and proof-of-principle experiments to demonstrate that endpoint quantifications can be fundamentally misleading because they overestimate defective phenotypes. Indeed, live-cell imaging reveals that, while depletion of dynein or the dynein binding protein Lis1 enables spindle formation in presence of an Eg5 inhibitor, the activities of dynein and Eg5 cannot be titrated against each other. Thus, dynein most likely antagonizes Eg5 indirectly by exerting force at different spindle locations rather than through a simple push-pull mechanism at the spindle equator.

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570 Biowissenschaften, Biologie
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ISO 690FLORIAN, Stefan, Thomas U. MAYER, 2012. The Functional Antagonism between Eg5 and Dynein in Spindle Bipolarization Is Not Compatible with a Simple Push-Pull Model. In: Cell Reports. 2012, 1(5), pp. 408-416. ISSN 2211-1247. eISSN 2211-1247. Available under: doi: 10.1016/j.celrep.2012.03.006
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@article{Florian2012-05-31Funct-21194,
  year={2012},
  doi={10.1016/j.celrep.2012.03.006},
  title={The Functional Antagonism between Eg5 and Dynein in Spindle Bipolarization Is Not Compatible with a Simple Push-Pull Model},
  number={5},
  volume={1},
  issn={2211-1247},
  journal={Cell Reports},
  pages={408--416},
  author={Florian, Stefan and Mayer, Thomas U.}
}
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