title: Depolymerizing kinesins Kip3 and MCAK shape cellular microtubule architecture by differential control of catastrophe.
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.
authors: Department of Genetics, University of Minnesota, Minneapolis, MN 55455, USA.
authors: Melissa K
authors: MK
authors: Gardner
authors: Marija
authors: M
authors: Zanic
authors: Christopher
authors: C
authors: Gell
authors: Volker
authors: V
authors: Bormuth
authors: Jonathon
authors: J
authors: Howard
mesh_terms: D000818:Animals; D002468:Cell Physiological Phenomena; D016922:Cellular Senescence; D006801:Humans; D016547:Kinesins / Q000378:metabolism*; D008870:Microtubules / Q000737:chemistry / Q000378:metabolism*; D014404:Tubulin / Q000378:metabolism
chemical_list: D014404:Tubulin; D016547:Kinesins