Depolymerizing kinesins Kip3 and MCAK shape cellular microtubule architecture by differential control of catastrophe - PubMed (original) (raw)

. 2011 Nov 23;147(5):1092-103.

doi: 10.1016/j.cell.2011.10.037.

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Depolymerizing kinesins Kip3 and MCAK shape cellular microtubule architecture by differential control of catastrophe

Melissa K Gardner et al. Cell. 2011.

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Abstract

Microtubules are dynamic filaments whose ends alternate between periods of slow growth and rapid shortening as they explore intracellular space and move organelles. A key question is how regulatory proteins modulate catastrophe, the conversion from growth to shortening. To study this process, we reconstituted microtubule dynamics in the absence and presence of the kinesin-8 Kip3 and the kinesin-13 MCAK. Surprisingly, we found that, even in the absence of the kinesins, the microtubule catastrophe frequency depends on the age of the microtubule, indicating that catastrophe is a multistep process. Kip3 slowed microtubule growth in a length-dependent manner and increased the rate of aging. In contrast, MCAK eliminated the aging process. Thus, both kinesins are catastrophe factors; Kip3 mediates fine control of microtubule length by narrowing the distribution of maximum lengths prior to catastrophe, whereas MCAK promotes rapid restructuring of the microtubule cytoskeleton by making catastrophe a first-order random process.

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