The Spindle Midzone Microtubule-Associated Proteins Ase1p and Cin8p Affect the Number and Orientation of Astral Microtubules in Saccharomyces cerevisiae

Gramont, Armand de; Barbour, Leslie; Ross, Karen; Cohen-Fix, Orna

doi:10.4161/cc.6.10.4181

Cited by 15 publications

(12 citation statements)

References 38 publications

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“…A recent report suggests that Cin8p plays a role in spindle positioning through an aMT-dependent mechanism, and so, coupled with our results for kMTs, we hypothesized that Cin8p also suppresses aMT assembly (de Gramont et al, 2007; Geiser et al, 1997). Using GFP-tubulin fluorescence microscopy, we measured the length of individual aMTs in the cytoplasm (Fig.…”

Section: Resultssupporting

confidence: 80%

Chromosome Congression by Kinesin-5 Motor-Mediated Disassembly of Longer Kinetochore Microtubules

Gardner

Bouck

Paliulis

et al. 2008

Cell

163

217

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Summary During mitosis, sister chromatids congress to the spindle equator and are subsequently segregated via attachment to dynamic kinetochore microtubule (kMT) plus-ends. A major question is how kMT plus-end assembly is spatially regulated to achieve chromosome congression. Here we find in budding yeast that the widely-conserved kinesin-5 sliding motor proteins, Cin8p and Kip1p, mediate chromosome congression by suppressing kMT plus-end assembly of longer kMTs. Of the two, Cin8p is the major effector and its activity requires a functional motor domain. In contrast, the depolymerizing kinesin-8 motor Kip3p plays a minor role in spatial regulation of yeast kMT assembly. Our analysis identified a model where kinesin-5 motors bind to kMTs, move to kMT plus ends, and upon arrival at a growing plus-end promote net kMT plus-end disassembly. In conclusion, we find that length-dependent control of net kMT assembly by kinesin-5 motors yields a simple and stable self-organizing mechanism for chromosome congression.

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Section: Resultssupporting

confidence: 80%

Chromosome Congression by Kinesin-5 Motor-Mediated Disassembly of Longer Kinetochore Microtubules

Gardner

Bouck

Paliulis

et al. 2008

Cell

163

217

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show abstract

“…The plausibility of such cooperation between an inner-spindlelocalized protein and a cortically-localized one is also supported by a growing body of evidence for interplay between the central spindle and cell cortex during anaphase, in high eukaryote as well as in S. cerevisiae cells [19,[74][75][76][77][78][79]. In this type of model, the cooperation between the inner-spindle Cin8 and the cortical dynein may involve, for example, a biochemical signaling similar to the one reported in HeLa cells, where an intracellular phosphorylation gradient was shown to be produced following the activation of Aurora B kinase, thereby allowing signaling from the midzone to the cell cortex [80].…”

Section: Discussionmentioning

confidence: 93%

Mid-anaphase arrest in S. cerevisiae cells eliminated for the function of Cin8 and dynein

Gerson-Gurwitz

Movshovich

Avunie

et al. 2008

Cell. Mol. Life Sci.

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S. cerevisiae anaphase spindle elongation is accomplished by the overlapping function of dynein and the kinesin-5 motor proteins, Cin8 and Kip1. Cin8 and dynein are synthetically lethal, yet the arrest phenotypes of cells eliminated for their function had not been identified. We found that at a non-permissive temperature, dyn1 Delta cells that carry a temperature-sensitive cin8 - 3 mutation arrest at mid-anaphase with a unique phenotype, which we named TAN (two microtubule asters in one nucleus). These cells enter anaphase, but fail to proceed through the slow phase of anaphase B. At a permissive temperature, dyn1 Delta, cin8 - 3 or dyn1 Delta cin8 - 3 cells exhibit perturbed spindle midzone morphologies, with dyn1Delta cin8 - 3 anaphase spindles also being profoundly bent and nonrigid. Sorbitol, which has been suggested to stabilize microtubules, corrects these defects and suppresses the TAN phenotype. We conclude that dynein and Cin8 cooperate in anaphase midzone organization and influence microtubule dynamics, thus enabling progression through the slow phase of anaphase B.

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“…We reasoned that other MT crosslinkers might become essential in the absence of Cut7. Ase1 is a non-essential antiparallel MT bundler, whose deletion results in metaphase spindle instability17182627 (Supplementary Fig. 3a), short spindle length at anaphase transition28 (Supplementary Fig.…”

Section: Resultsmentioning

confidence: 99%

Kinesin-5-independent mitotic spindle assembly requires the antiparallel microtubule crosslinker Ase1 in fission yeast

et al. 2017

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Bipolar spindle assembly requires a balance of forces where kinesin-5 produces outward pushing forces to antagonize the inward pulling forces from kinesin-14 or dynein. Accordingly, Kinesin-5 inactivation results in force imbalance leading to monopolar spindle and chromosome segregation failure. In fission yeast, force balance is restored when both kinesin-5 Cut7 and kinesin-14 Pkl1 are deleted, restoring spindle bipolarity. Here we show that the cut7Δpkl1Δ spindle is fully competent for chromosome segregation independently of motor activity, except for kinesin-6 Klp9, which is required for anaphase spindle elongation. We demonstrate that cut7Δpkl1Δ spindle bipolarity requires the microtubule antiparallel bundler PRC1/Ase1 to recruit CLASP/Cls1 to stabilize microtubules. Brownian dynamics-kinetic Monte Carlo simulations show that Ase1 and Cls1 activity are sufficient for initial bipolar spindle formation. We conclude that pushing forces generated by microtubule polymerization are sufficient to promote spindle pole separation and the assembly of bipolar spindle in the absence of molecular motors.

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The Spindle Midzone Microtubule-Associated Proteins Ase1p and Cin8p Affect the Number and Orientation of Astral Microtubules in Saccharomyces cerevisiae

Cited by 15 publications

References 38 publications

Chromosome Congression by Kinesin-5 Motor-Mediated Disassembly of Longer Kinetochore Microtubules

Chromosome Congression by Kinesin-5 Motor-Mediated Disassembly of Longer Kinetochore Microtubules

Mid-anaphase arrest in S. cerevisiae cells eliminated for the function of Cin8 and dynein

Kinesin-5-independent mitotic spindle assembly requires the antiparallel microtubule crosslinker Ase1 in fission yeast

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