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

Histone Variants at the Centromere02:30

Histone Variants at the Centromere

4.6K
Histone variants are the histone proteins with structural and sequence variations. These variants may be regarded as “mutant” forms that replace their canonical histone counterparts in the nucleosomes. Specific post-translational modifications on the histone variants enable further chromatin complexity and regulate tissue-specific gene expression. The most common histone variants are from histone H2A, H2B, and linker histone H1 families. However, several variants of histone H3...
4.6K
Centrosome Duplication02:25

Centrosome Duplication

4.2K
The primary microtubule organizing center (MTOC) in animal cells is the centrosome. A centrosome has two cylindrical centrioles at its core. Each centriole consists of nine sets of three microtubules held together by proteins. The centrioles are positioned at right angles to each other and surrounded by a shapeless protein cloud called the pericentriolar matrix, or pericentriolar material (PCM).
To ensure that each daughter cell receives a centrosome after cell division, centrosome duplication...
4.2K
Attachment of Sister Chromatids02:57

Attachment of Sister Chromatids

3.5K
As cells progress into mitosis, the nuclear envelope breaks down, and the condensed chromosomes are exposed to the array of bipolar microtubules of the mitotic spindle. The kinetochore, a large, disc-shaped protein complex, is present at the centromere region of the sister chromatids and acts as a binding site for the microtubules.  Usually, the plus-end of a single microtubule is embedded within the kinetochore. However, some kinetochores first establish lateral contact with the side-wall...
3.5K
The Spindle Assembly Checkpoint02:19

The Spindle Assembly Checkpoint

3.3K
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...
3.3K
Spindle Assembly02:50

Spindle Assembly

3.9K
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...
3.9K
Anaphase A and B01:39

Anaphase A and B

4.3K
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...
4.3K

You might also read

Related Articles

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

Sort by
Same author

Implementation of Measurement-Based Care in Mental Health Services: A Systematic Literature Review.

Psychiatric services (Washington, D.C.)·2026
Same author

Stakeholder insights into hospital-home transitions for older adults in a decentralised health system: a qualitative study.

BMC health services research·2026
Same author

Chromatin architectures underlying plasmid-based assays for regulatory variant effects.

Molecular cell·2026
Same author

Genome instability triggers intercellular DNA transfer between human cells.

Cell·2026
Same author

A unified photosensitizer platform for <i>in situ</i> DNA-, RNA-, and protein-directed proximity labeling.

bioRxiv : the preprint server for biology·2026
Same author

Development and internal validation of a 30-day readmission risk model for older adults using Swiss electronic health record data: a retrospective cohort study.

BMC geriatrics·2026

Related Experiment Video

Updated: Oct 26, 2025

Mass Spectrometry Analysis to Identify Ubiquitylation of EYFP-tagged CENP-A EYFP-CENP-A
09:02

Mass Spectrometry Analysis to Identify Ubiquitylation of EYFP-tagged CENP-A EYFP-CENP-A

Published on: June 10, 2020

5.7K

Suv420 enrichment at the centromere limits Aurora B localization and function.

Conor P Herlihy1, Sabine Hahn1, Nicole M Hermance1

  • 1Department of Biology and Biotechnology, Worcester Polytechnic Institute, Worcester, MA, 01609USA.

Journal of Cell Science
|August 3, 2021
PubMed
Summary

Overexpression of Suv39 and Suv420 enzymes at centromeres disrupts chromosome segregation by affecting Aurora B localization. Inhibiting Suv420 can restore proper cell division, suggesting a role in cancer.

Keywords:
CentromereChromosome instabilityMitosis

More Related Videos

Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins
05:35

Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins

Published on: March 3, 2016

15.4K
Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells
06:29

Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells

Published on: July 30, 2020

3.2K

Related Experiment Videos

Last Updated: Oct 26, 2025

Mass Spectrometry Analysis to Identify Ubiquitylation of EYFP-tagged CENP-A EYFP-CENP-A
09:02

Mass Spectrometry Analysis to Identify Ubiquitylation of EYFP-tagged CENP-A EYFP-CENP-A

Published on: June 10, 2020

5.7K
Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins
05:35

Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins

Published on: March 3, 2016

15.4K
Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells
06:29

Real-Time Monitoring of Aurora kinase A Activation using Conformational FRET Biosensors in Live Cells

Published on: July 30, 2020

3.2K

Area of Science:

  • Epigenetics and Molecular Biology
  • Cell Biology
  • Cancer Research

Background:

  • Centromere function relies on epigenetic histone modifications, particularly H3K9me3 and H4K20me3 in pericentromeric heterochromatin.
  • Misregulation of methyltransferases Suv39 and Suv420, which establish these marks, is implicated in disease but not fully understood.

Purpose of the Study:

  • To investigate the functional consequences of aberrant centromeric localization of Suv39 and Suv420.
  • To determine the impact of these epigenetic modifications on centromere transcription and mitotic fidelity.

Main Methods:

  • Analysis of centromere localization of Suv39 and Suv420.
  • Assessment of centromere transcription levels.
  • Evaluation of Aurora B kinase localization and microtubule dynamics.
  • Investigation of chromosome alignment and segregation accuracy.
  • Pharmacological inhibition of Suv420 methyltransferase activity.

Main Results:

  • Increased centromere localization of Suv39 and Suv420 suppressed centromere transcription and Aurora B localization.
  • This led to reduced microtubule dynamics, impaired chromosome alignment, and errors in segregation.
  • Inhibition of Suv420 partially restored Aurora B to centromeres, correcting mitotic errors.
  • High expression of Suv39/Suv420 correlated with sensitivity to Aurora kinase inhibitors in cancer cells.

Conclusions:

  • Aberrant centromeric enrichment of H3K9me3 and H4K20me3, mediated by Suv39 and Suv420, disrupts mitotic progression by negatively regulating Aurora B.
  • This epigenetic dysregulation is a potential driver of chromosome mis-segregation in cancer.
  • Targeting Suv420 activity may offer therapeutic strategies for cancers with elevated H3K9/H4K20 methylation.