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Related Concept Videos

Centrosome Duplication02:25

Centrosome Duplication

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...
Centrosome Duplication02:25

Centrosome Duplication

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...
Centrioles and Centrosomes01:13

Centrioles and Centrosomes

Most animal cells comprise a pair of centrioles together called a centrosome. The cell duplicates its centrosome and contains two centrosomes side-by-side, which begin to move apart during the prophase. As the centrosomes migrate to two different sides of the cell, microtubules start extending from each centrosome toward the other end. The mitotic spindle is composed of the centrosomes and their emerging microtubules.
Near the end of the prophase, also called late prophase or "prometaphase,"...
Autophagy01:27

Autophagy

Autophagy is a self-digesting process by which a cell protects itself from threats both within and outside the cell, ranging from abnormal proteins to invading bacteria. In this process, obsolete components of the cell and invading microbes are degraded by hydrolytic enzymes active in an acidic environment of the lysosomal lumen.
An autophagic pathway consists of a series of signaling events activated in response to diverse stress and physiological conditions such as food deprivation,...
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...
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: Jun 23, 2026

Quantitative Immunofluorescence Assay to Measure the Variation in Protein Levels at Centrosomes
09:39

Quantitative Immunofluorescence Assay to Measure the Variation in Protein Levels at Centrosomes

Published on: December 20, 2014

Sensing centrosome amplification: the interface between centriole duplication and autophagy.

Paula A Coelho1,2, Agnieszka Fatalska3, Marco Geymonat3

  • 1Division of Biology and Biological Engineering, California Institute of Technology, Pasadena, CA, USA. palmeida@caltech.edu.

Nature Communications
|June 21, 2026
PubMed
Summary

Cells can overcome proliferation arrest caused by extra centrosomes by downregulating specific pathways. The tumor suppressor ARHGAP15 activates autophagy to reduce centrosomes and enable cell proliferation.

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

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Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins
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Immunofluorescence Analysis of Endogenous and Exogenous Centromere-kinetochore Proteins

Published on: March 3, 2016

Related Experiment Videos

Last Updated: Jun 23, 2026

Quantitative Immunofluorescence Assay to Measure the Variation in Protein Levels at Centrosomes
09:39

Quantitative Immunofluorescence Assay to Measure the Variation in Protein Levels at Centrosomes

Published on: December 20, 2014

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

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

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Genetics

Background:

  • Multipolar mitotic spindles with extra centrosomes are observed in cancer cells but poorly understood.
  • Centrosome amplification can impose proliferation arrest in cells.

Purpose of the Study:

  • To identify pathways that enable cell proliferation despite centrosome amplification.
  • To investigate the role of the tumor suppressor ARHGAP15 in overcoming centrosome amplification-induced proliferation arrest.

Main Methods:

  • Genome-wide screen to identify pathways involved in proliferation.
  • Depletion of ARHGAP15 and assessment of its effects on centrosome number and cell proliferation.
  • Investigation of the interaction between ARHGAP15 and autophagy protein ATG16L1.
  • Analysis of the ARHGAP15-ARHGEF2-RAC1 pathway.

Main Results:

  • Downregulation of Wnt, Hippo, p53, PIDDosome, ciliary biogenesis, or autophagy pathways enables proliferation of cells with PLK4-mediated centrosome amplification.
  • Depletion of ARHGAP15 activates autophagy, overcomes centrosome amplification, and enables embryonic fibroblast proliferation.
  • Reduction of centrosomes after ARHGAP15 depletion requires ATG16L1 and involves ARHGAP15 association with ATG16L1 when autophagy is inactive.
  • ARHGAP15 is opposed by ARHGEF2, which is activated by CEP170 to promote RAC1-GTP generation and autophagy.

Conclusions:

  • Specific pathway downregulation allows cells to proliferate despite centrosome amplification.
  • ARHGAP15 acts as a tumor suppressor by activating autophagy, reducing centrosome numbers, and promoting proliferation.
  • The ARHGAP15-ARHGEF2-CEP170-RAC1 axis plays a crucial role in regulating autophagy and cytoskeletal dynamics.