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Related Concept Videos

Anaphase A and B01:39

Anaphase A and B

Microtubules form through the end-to-end polymerization of tubulin heterodimers. Kinetochore microtubules originate from the spindle poles, and their plus-ends connect with the kinetochores on sister-chromatids. Ndc80 protein complexes, present on the kinetochore, form low-affinity links with the plus end of these kinetochore microtubules.
Plus-end depolymerization releases tubulin heterodimers from the terminal region of the microtubule. As tubulin subunits are lost, the Ndc80 complexes detach...
Destabilization of Microtubules01:45

Destabilization of Microtubules

The destabilization of microtubules can occur during different stages of the microtubule lifecycle, such as nucleation or elongation. It can take place at either end of the microtubule or in the microtubule lattices as a whole. The lifespan of individual microtubules within a cell varies according to the cell type and stage of the cell cycle. During interphase, the lifespan of the microtubule is about 30 minutes, while during cell division, it is about 15 minutes. In axonal microtubules of...
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

At the transition from prophase to metaphase, there is a reduction in cohesion along the chromosomal arms, resulting in the resolution of sister chromatids. However, residual cohesin connections remain to hold the sister chromatids together until the transition from metaphase to anaphase. The residual connection prevents any premature separation of sister chromatids, blocking the risks of aneuploidy within the daughter cells.
At the onset of anaphase, separase, a proteolytic enzyme, is...
The Spindle Assembly Checkpoint02:19

The Spindle Assembly Checkpoint

The spindle assembly checkpoint is a molecular surveillance mechanism ensuring the fidelity of chromosome segregation during anaphase. The checkpoint monitors the completion of all the prerequisite steps before chromosome segregation to determine whether the segregation process should proceed or be delayed.
Many proteins function together to control the spindle assembly checkpoint. Mutations affecting these proteins may allow cells to proceed into anaphase prematurely, resulting in the...
Forces Acting on Chromosomes02:11

Forces Acting on Chromosomes

During mitosis, chromosome movements occur through the interplay of multiple piconewton level forces. In prometaphase, these forces help in chromosome assembly or congression at the equatorial plane, eventually leading to their alignment at the metaphase plate. The forces acting on the chromosomes are space and time-dependent; therefore, they vary with the position of the chromosomes as the cell progresses through mitosis. 
Microtubules and motor proteins exert two types of forces on...
Anaphase Promoting Complex00:50

Anaphase Promoting Complex

The stepwise destruction of specific proteins is necessary for the progression and completion of the cell cycle. Such proteins are ubiquitinated by ubiquitin ligases and then subsequently destroyed by the proteasome. The SCF (Skp1/Cullin/F-box) and the anaphase-promoting complex (APC) are two important ubiquitin ligases involved in cell cycle progression. While SCF is active throughout the cell cycle, APC gets activated during metaphase to anaphase transition. Cdc20 or Cdh1 binds to APC and...

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Related Experiment Video

Updated: Jul 3, 2026

Generating a "Humanized" Drosophila S2 Cell Line Sensitive to Pharmacological Inhibition of Kinesin-5
11:09

Generating a "Humanized" Drosophila S2 Cell Line Sensitive to Pharmacological Inhibition of Kinesin-5

Published on: January 20, 2016

Slk19-dependent mid-anaphase pause in kinesin-5-mutated cells.

Natalia Movshovich1, Vladimir Fridman, Adina Gerson-Gurwitz

  • 1Department of Chemistry, Ben-Gurion University of the Negev, Beer-Sheva, Israel.

Journal of Cell Science
|July 17, 2008
PubMed
Summary
This summary is machine-generated.

Mutations in kinesin-5 motor proteins in yeast cells disrupt anaphase spindle elongation, causing a mid-anaphase pause. This pause, dependent on Slk19, may ensure proper DNA segregation.

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Use of Time-Lapse Microscopy and Stage-Specific Nuclear Depletion of Proteins to Study Meiosis in S. cerevisiae
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Live Cell Imaging to Assess the Dynamics of Metaphase Timing and Cell Fate Following Mitotic Spindle Perturbations
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Generating a "Humanized" Drosophila S2 Cell Line Sensitive to Pharmacological Inhibition of Kinesin-5
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Use of Time-Lapse Microscopy and Stage-Specific Nuclear Depletion of Proteins to Study Meiosis in S. cerevisiae
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Live Cell Imaging to Assess the Dynamics of Metaphase Timing and Cell Fate Following Mitotic Spindle Perturbations
07:14

Live Cell Imaging to Assess the Dynamics of Metaphase Timing and Cell Fate Following Mitotic Spindle Perturbations

Published on: September 20, 2019

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Kinesin-5 motor proteins are crucial for spindle assembly and function.
  • Anaphase spindle elongation is a critical process for chromosome segregation.
  • The FEAR pathway regulates early-anaphase events, including Cdc14 phosphatase activation.

Purpose of the Study:

  • To investigate the role of kinesin-5 motor proteins (Cin8 and Kip1) in anaphase spindle elongation in Saccharomyces cerevisiae.
  • To determine the impact of specific kinesin-5 mutations on spindle dynamics and midzone organization.
  • To explore the involvement of FEAR pathway components and the pre-anaphase checkpoint in regulating spindle elongation defects.

Main Methods:

  • Yeast genetics: construction of kip1 deletion and expression of Cin8 motor-domain mutants (Cin8-F467A, Cin8-R196K).
  • Microscopy to observe anaphase spindle elongation and midzone structure.
  • Genetic manipulation of FEAR pathway components (SLK19, SPO12) and Cdc20 to assess their effects.

Main Results:

  • Kinesin-5 mutations, particularly in kip1 Delta cin8-F467A cells, led to interrupted spindle elongation and a mid-anaphase pause.
  • Mutant cells exhibited asymmetric midzone location and enlarged midzone size, indicating impaired organization.
  • Deletion of SLK19, but not SPO12, abolished the mid-anaphase pause, induced premature anaphase onset, and caused DNA division defects.
  • Overexpression of Cdc20 also eliminated the pause but resulted in DNA deformation.

Conclusions:

  • Proper kinesin-5 function and midzone organization are essential for continuous anaphase spindle elongation.
  • A Slk19-dependent mid-anaphase pause, potentially triggered by pre-anaphase checkpoint activation in kinesin-5 mutants, may be vital for accurate DNA segregation.