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

Apoptosis01:30

Apoptosis

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 reduction of the tissue.
The Intrinsic Apoptotic Pathway01:31

The Intrinsic Apoptotic Pathway

Internal cellular stress, such as cellular injury or hypoxia, triggers intrinsic apoptosis. The B-cell lymphoma 2 (Bcl-2) family of proteins are the primary regulators of the intrinsic apoptotic pathway. For example, during DNA damage, checkpoint proteins, such as Ataxia Telangiectasia Mutated (ATM protein) and Checkpoints Factor-2 (Chk2) proteins, are activated. These proteins phosphorylate p53 which further activates pro-apoptotic proteins, such as Bax, Bak, PUMA, and Noxa, and inhibits...
Autophagic Cell Death01:18

Autophagic Cell Death

Christian de Duve discovered “autophagy,” a process in which cellular components are engulfed by membrane-bound organelles called autophagosomes. The autophagosomes then fuse with lysosomes to digest the enclosed contents. Autophagy is generally activated in cells to prevent cell death. However, cell death is triggered when the damage is beyond repair.
Autophagy and Apoptosis
Autophagy can activate apoptosis. In normal conditions, the autophagy activating protein Beclin-1 and pro-apoptotic...
The Extrinsic Apoptotic Pathway01:17

The Extrinsic Apoptotic Pathway

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...
Yeast Signaling01:28

Yeast Signaling

Yeasts are single-celled organisms, but unlike bacteria, they are eukaryotes (cells with a nucleus). Cell signaling in yeast is similar to signaling in other eukaryotic cells. A ligand, such as a protein or a small molecule released from a yeast cell, attaches to a receptor on the cell surface. The binding stimulates second-messenger kinases to activate or inactivate transcription factors that further regulate gene expression. Many of the yeast intracellular signaling cascades have similar...
Cellular Injury V: Apoptosis and Autophagy01:22

Cellular Injury V: Apoptosis and Autophagy

Cells respond to damage and stress through highly coordinated processes that decide whether they survive or undergo controlled self-destruction. Two major pathways involved in this regulation are apoptosis, a type of programmed cell death, and autophagy, a survival mechanism that helps cells adapt to adverse conditions.ApoptosisApoptosis removes aged or injured cells to maintain tissue balance. During this process, the cell shrinks, chromatin condenses and fragments, and membrane-bound...

You might also read

Related Articles

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

Sort by
Same author

<i>SLC4A1</i> mutations that cause distal renal tubular acidosis alter cytoplasmic pH and cellular autophagy.

eLife·2026
Same author

Correction for Gier et al., "Analysis of Yeast Killer Toxin K1 Precursor Processing via Site-Directed Mutagenesis: Implications for Toxicity and Immunity".

mSphere·2025
Same author

Responses Toward Injustice Shaped by Justice Sensitivity - Evidence From Germany.

Frontiers in psychology·2022
Same author

Boosting endoplasmic reticulum folding capacity reduces unfolded protein response activation and intracellular accumulation of human kidney anion exchanger 1 in Saccharomyces cerevisiae.

Yeast (Chichester, England)·2021
Same author

Cell-type-specific differences in KDEL receptor clustering in mammalian cells.

PloS one·2020
Same author

Analysis of Yeast Killer Toxin K1 Precursor Processing via Site-Directed Mutagenesis: Implications for Toxicity and Immunity.

mSphere·2020

Related Experiment Video

Updated: Jul 7, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Viral induced yeast apoptosis.

Manfred J Schmitt1, Jochen Reiter

  • 1Molecular and Cell Biology, FR 8.3 Biosciences, Saarland University, Saarbrücken, Germany. mjs@microbiol.uni-sb.de

Biochimica Et Biophysica Acta
|February 23, 2008
PubMed
Summary

Yeast programmed cell death (PCD) can be triggered by viral killer toxins and pathogens. These toxins, even at low doses, induce apoptosis, conferring a survival advantage to killer yeast strains.

Area of Science:

  • * Microbiology and molecular biology
  • * Cellular biology and programmed cell death (PCD)
  • * Virology and yeast genetics

Background:

  • * Yeast programmed cell death (PCD) is induced by various factors, including viral agents.
  • * Killer yeast strains harbor double-stranded RNA viruses, enabling toxin production and secretion.
  • * These viral toxins exhibit diverse mechanisms, targeting cell membranes or nuclear functions.

Purpose of the Study:

  • * To investigate the role of viral killer toxins and pathogens in inducing PCD in yeast.
  • * To elucidate the mechanisms by which viral toxins trigger cell death pathways.
  • * To understand the ecological implications of viral-induced PCD in yeast populations.

Main Methods:

  • * Analysis of yeast strains infected with dsRNA viruses.

More Related Videos

Evaluation of Caspase Activation to Assess Innate Immune Cell Death
10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

Related Experiment Videos

Last Updated: Jul 7, 2026

Yeast As a Chassis for Developing Functional Assays to Study Human P53
14:57

Yeast As a Chassis for Developing Functional Assays to Study Human P53

Published on: August 4, 2019

Evaluation of Caspase Activation to Assess Innate Immune Cell Death
10:23

Evaluation of Caspase Activation to Assess Innate Immune Cell Death

Published on: January 20, 2023

  • * Characterization of viral toxin structures and functions (e.g., pore-forming, nuclear-acting).
  • * Assessment of cell death induction (necrosis vs. apoptosis) at varying toxin concentrations.

    • Main Results:

    • * Viral toxins induce necrotic cell death at high concentrations and caspase- and ROS-mediated apoptosis at lower concentrations.
    • * Killer yeast strains are immune to their own secreted toxins.
    • * Killer viruses themselves can induce apoptosis in non-infected yeast cells.

    Conclusions:

    • * Viral toxins are potent inducers of PCD in sensitive yeast cells, even at sub-lethal doses.
    • * Viral-induced PCD provides a competitive advantage to killer yeast, facilitating dominance.
    • * Yeast-pathogen interactions involving viral toxins and PCD are crucial for microbial ecology.