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.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 1092-1103 |
| Number of pages | 12 |
| Journal | Cell |
| Volume | 147 |
| Issue number | 5 |
| DOIs | |
| State | Published - Nov 23 2011 |
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Depolymerizing kinesins Kip3 and MCAK shape cellular microtubule architecture by differential control of catastrophe. / Gardner, Melissa K.; Zanic, Marija; Gell, Christopher; Bormuth, Volker; Howard, Jonathon.
In: Cell, Vol. 147, No. 5, 23.11.2011, p. 1092-1103.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Depolymerizing kinesins Kip3 and MCAK shape cellular microtubule architecture by differential control of catastrophe
AU - Gardner, Melissa K.
AU - Zanic, Marija
AU - Gell, Christopher
AU - Bormuth, Volker
AU - Howard, Jonathon
PY - 2011/11/23
Y1 - 2011/11/23
N2 - 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.
AB - 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.
UR - http://www.scopus.com/inward/record.url?scp=81855189480&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=81855189480&partnerID=8YFLogxK
U2 - 10.1016/j.cell.2011.10.037
DO - 10.1016/j.cell.2011.10.037
M3 - Article
C2 - 22118464
AN - SCOPUS:81855189480
VL - 147
SP - 1092
EP - 1103
JO - Cell
JF - Cell
SN - 0092-8674
IS - 5
ER -