Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Concept Videos

The Spindle Assembly Checkpoint02:19

The Spindle Assembly Checkpoint

3.9K
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...
3.9K
Meiosis II02:02

Meiosis II

50.9K
Meiosis II entails cell division and segregation of the sister chromatids, resulting in the production of four unique haploid gametes. The steps for meiosis II are similar to mitosis, except that meiosis II occurs in haploid cells, whereas mitosis occurs in diploid cells.
The timing and cell division patterns of meiosis differ between males and females. In male meiosis, the centrosomes are part of the formation of the meiotic spindle. However, in oocytes, including that of humans, Drosophila,...
50.9K
Spindle Assembly02:50

Spindle Assembly

4.4K
Spindle assembly occurs through three, often coexisting, pathways – the centrosome-mediated pathway, the chromatin-mediated pathway, and the microtubule-mediated pathway – collectively contributing to form a robust spindle apparatus.
In most cells, centrosomes are the primary microtubule nucleation centers. In the centrosome-mediated pathway, the G2-prophase transition triggers centrosome maturation and increased microtubule nucleation. Progressive nucleation results in a...
4.4K
Separation of Sister Chromatids02:17

Separation of Sister Chromatids

4.6K
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...
4.6K
Anaphase A and B01:39

Anaphase A and B

5.6K
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...
5.6K
The Mitotic Spindle02:27

The Mitotic Spindle

8.2K
The mitotic spindle—or spindle apparatus—is a eukaryotic, cytoskeletal structure made up of long protein fibers called microtubules. Formed during cell division, the spindle separates sister chromatids and moves them to opposite ends of a parental cell, where the now individual chromosomes are distributed to two daughter cell nuclei.
The bipolar configuration of the mitotic spindle facilitates chromosomal segregation, preparing the cell for division. One mechanism that ensures...
8.2K

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Development of in vitro airway epithelial model to assess immune response and safety of mucosal adjuvants.

NPJ vaccines·2026
Same author

HSV ICP27 hijacks host splicing factor SRSF3 to regulate pre-mRNA splicing and export for viral gene expression and immune evasion.

PLoS pathogens·2026
Same author

Human neutrophils are a cellular source of apolipoprotein A-I.

Journal of leukocyte biology·2025
Same author

Insights into regulatory T-cell and type-I interferon roles in determining abacavir-induced hypersensitivity or immune tolerance.

Frontiers in immunology·2025
Same author

Endothelial PHD2 deficiency induces apoptosis resistance and inflammation via AKT activation and AIP1 loss independent of HIF2α.

American journal of physiology. Lung cellular and molecular physiology·2024
Same author

Recombinant OC43 SARS-CoV-2 spike replacement virus: An improved BSL-2 proxy virus for SARS-CoV-2 neutralization assays.

Proceedings of the National Academy of Sciences of the United States of America·2024

Related Experiment Video

Updated: Mar 1, 2026

Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes
10:09

Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes

Published on: September 13, 2022

2.6K

PP2A-B56γ is required for an efficient spindle assembly checkpoint.

Prajakta Varadkar1, Fatima Abbasi1, Kazuyo Takeda1

  • 1a Division of Cellular and Gene Therapies, Center for Biologics Evaluation and Research , US Food and Drug Administration , Silver Spring , MD.

Cell Cycle (Georgetown, Tex.)
|June 1, 2017
PubMed
Summary

The Spindle Assembly Checkpoint (SAC) requires PP2A-B56γ to stabilize BubR1, preventing premature cell division. Loss of PP2A-B56γ leads to chromosomal instability, a cancer hallmark.

Keywords:
B56B56gammaBUBR1PP2APP2A-B56SACspindle assembly checkpoint

More Related Videos

Manipulation and Analysis of Cell Cycle-Dependent Processes in Budding Yeast
08:13

Manipulation and Analysis of Cell Cycle-Dependent Processes in Budding Yeast

Published on: September 26, 2025

634
Live Cell Imaging of Chromosome Segregation During Mitosis
06:39

Live Cell Imaging of Chromosome Segregation During Mitosis

Published on: March 14, 2018

9.9K

Related Experiment Videos

Last Updated: Mar 1, 2026

Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes
10:09

Evaluation of the Spindle Assembly Checkpoint Integrity in Mouse Oocytes

Published on: September 13, 2022

2.6K
Manipulation and Analysis of Cell Cycle-Dependent Processes in Budding Yeast
08:13

Manipulation and Analysis of Cell Cycle-Dependent Processes in Budding Yeast

Published on: September 26, 2025

634
Live Cell Imaging of Chromosome Segregation During Mitosis
06:39

Live Cell Imaging of Chromosome Segregation During Mitosis

Published on: March 14, 2018

9.9K

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • The Spindle Assembly Checkpoint (SAC) ensures accurate chromosome segregation during mitosis.
  • BubR1 is crucial for SAC function, preventing premature anaphase onset.
  • Protein phosphatases, including PP2A, regulate SAC activity.

Purpose of the Study:

  • To investigate the role of PP2A-B56γ in maintaining BubR1 stability during cell cycle arrest.
  • To determine if PP2A-B56γ inactivation impacts SAC efficiency and chromosomal integrity.
  • To explore the functional redundancy of PP2A-B56 family members.

Main Methods:

  • Utilized nocodazole to induce cell cycle arrest.
  • Examined BubR1 protein stability in primary cells lacking B56γ.
  • Assessed chromosomal segregation accuracy in cells with altered PP2A-B56γ function.
  • Investigated the subcellular localization of different B56 subunits.

Main Results:

  • PP2A-B56γ is essential for BubR1 stability during nocodazole-induced arrest.
  • Primary cells lacking B56γ exhibit premature BubR1 degradation and proceed through mitosis.
  • Inactivation of PP2A-B56γ alone impairs SAC efficiency, leading to abnormal chromosomal segregation.
  • Differential subcellular localization of B56 subunits suggests non-redundant functions.

Conclusions:

  • PP2A-B56γ plays a critical, non-redundant role in SAC regulation by stabilizing BubR1.
  • Disruption of PP2A-B56γ function compromises genomic stability, potentially contributing to tumorigenesis.
  • The distinct localization patterns of B56 subunits support their specialized roles within the SAC pathway.