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Related Concept Videos

Caspases01:24

Caspases

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Caspase, a family of cysteine proteases, serve as effectors in apoptosis. The ced3 gene in C.elegans was first identified to be involved in apoptosis. This gene encodes the ced-3 caspase that is similar to the interleukin-1-beta converting enzyme or ICE in mammals. In addition to apoptosis, caspases also function in the inflammatory response. Inflammatory caspases are essential in activating pro-inflammatory cytokines that recruit immune cells and block the replication of pathogens inside...
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Centrosome Duplication02:25

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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).
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Centrioles and Centrosomes01:13

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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.
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The Extrinsic Apoptotic Pathway01:17

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The extrinsic apoptotic pathway is initiated when extracellular death-inducing signals, such as specific cytokines, activate the death receptors expressed on the cell surface. The immune cells involved in this pathway are natural killer cells (NK cells) and cytotoxic T-lymphocytes. NK cells are critical in innate immune response, while cytotoxic T-lymphocytes are associated with adaptive immune response. These cells recognize specific receptors expressed on the altered cells and activate...
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Apoptosis01:30

Apoptosis

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Apoptosis is a combination of two Greek words, 'apo' and 'ptosis,' meaning separation and falling off, respectively. Hippocrates used this word to describe gangrene, which was caused due to bandaging of fractured bones. Apoptosis was distinguished from necrosis in 1970 when John Kerr reported observations of morphological changes occurring during apoptosis. During one experiment, he observed that the disruption of blood supply to the liver tissue resulted in a size...
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Separation of Sister Chromatids02:17

Separation of Sister Chromatids

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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.
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Cell Death Associated with Abnormal Mitosis Observed by Confocal Imaging in Live Cancer Cells
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Caspase-2 kills cells with extra centrosomes.

Dario Rizzotto1, Vincenza Vigorito2, Patricia Rieder1

  • 1CeMM Research Center for Molecular Medicine of the Austrian Academy of Sciences, 1090 Vienna, Austria.

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|October 30, 2024
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Summary
This summary is machine-generated.

Extra centrosomes trigger caspase-2-driven apoptosis in blood cells that fail cytokinesis, preventing pathogenic polyploidization. This cell death pathway involves the PIDDosome complex and BID processing, highlighting the centrosome

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Strategies for Tracking Anastasis, A Cell Survival Phenomenon that Reverses Apoptosis
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Area of Science:

  • Cell Biology
  • Molecular Biology
  • Apoptosis Research

Background:

  • Centrosomes are crucial microtubule organizing centers essential for cell function.
  • Uncontrolled centrosome duplication can lead to genomic instability and disease.
  • Cytokinesis failure can result in polyploidization, a state linked to pathogenesis.

Purpose of the Study:

  • To investigate the role of centrosomes in cell death following cytokinesis failure.
  • To elucidate the molecular mechanisms linking extra centrosomes to apoptosis.
  • To understand how cells prevent pathogenic polyploidization.

Main Methods:

  • Analysis of blood cells undergoing cytokinesis failure.
  • Investigating caspase-2 activation and its dependence on the PIDDosome complex.
  • Utilizing genetic manipulation (e.g., ANKRD26, BID deficiency) to study cell survival and apoptosis.
  • Examining mitochondrial outer membrane permeabilization (MOMP) and p53-dependent pathways.

Main Results:

  • Extra centrosomes are necessary to trigger caspase-2-driven apoptosis in cells failing cytokinesis.
  • Priming of PIDD1 at extra centrosomes is critical for caspase-2 pathway activation.
  • Loss of ANKRD26 permits cell survival and polyploidization.
  • Caspase-2 processes BID, initiating BAX/BAK-dependent MOMP.
  • BID-deficient cells activate p53-dependent apoptosis via caspase-2.

Conclusions:

  • Centrosomes limit their own unscheduled duplication by inducing PIDDosome-driven apoptosis.
  • This mechanism prevents potentially pathogenic polyploidization events.
  • The study reveals a novel role for centrosomes in regulating cell fate and preventing aneuploidy.