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Updated: Nov 23, 2025

Preparation of Meiotic Chromosome Spreads from Mouse Oocytes for Assessment of Synapsis and Recombination

Preparation of Meiotic Chromosome Spreads from Mouse Oocytes for Assessment of Synapsis and Recombination

Published on: July 18, 2025

chTOG is a conserved mitotic error correction factor.

Jacob A Herman¹, Matthew P Miller¹, Sue Biggins¹

¹Howard Hughes Medical Institute, Division of Basic Sciences, Fred Hutchinson Cancer Research Center, Seattle, United States.

|December 30, 2020

Summary

This summary is machine-generated.

The TOG protein family, including chTOG, provides intrinsic error correction for kinetochore-microtubule attachments. This ensures accurate chromosome segregation by stabilizing correct attachments and destabilizing incorrect ones.

Keywords:

Aurora B S. cerevisiae cell biology chTOG error correction human kinetochore microtubule mitosis

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Area of Science:

Cell Biology
Molecular Biology
Genetics

Background:

Accurate chromosome segregation is crucial for cell division.
Kinetochores must attach to microtubules from opposite spindle poles (biorientation) to achieve tension.
Initial kinetochore-microtubule attachments are often erroneous and require correction.

Purpose of the Study:

To investigate the role of the TOG protein family in kinetochore-microtubule attachment stability.
To determine if TOG proteins contribute to intrinsic error correction mechanisms.
To elucidate the function of chTOG in kinetochore-microtubule dynamics and error correction.

Main Methods:

Utilized budding yeast and human cell lines.
Investigated protein interactions, specifically chTOG with Hec1.
Generated and analyzed chTOG mutants affecting microtubule dynamics.
Assessed kinetochore-microtubule attachment stability and Aurora B activity.

Main Results:

Low-tension kinetochore-microtubule attachments are intrinsically less stable than high-tension ones.
The TOG protein Stu2 is required for this intrinsic tension-sensitive behavior.
Human chTOG localizes to kinetochores via Hec1 interaction, independent of microtubules.
A chTOG mutant disrupted error correction, leading to persistent erroneous attachments insensitive to Aurora B.

Conclusions:

TOG proteins, including chTOG, possess an intrinsic error correction activity at kinetochores.
This activity is independent of Aurora B kinase and contributes to accurate chromosome segregation.
TOG proteins are essential regulators of kinetochore-microtubule attachment fidelity.