Related Experiment Video

Updated: Jun 26, 2026

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

Human initiator caspases trigger apoptotic and autophagic phenotypes in Saccharomyces cerevisiae

Patricia Lisa-Santamaría1, Aaron M Neiman, Alvaro Cuesta-Marbán

  • 1Instituto de Microbiología Bioquímica y Departamento de Microbiología y Genética, CSIC/Universidad de Salamanca, Campus Miguel de Unamuno, E-37007 Salamanca, Spain.

Biochimica Et Biophysica Acta
|January 27, 2009
PubMed

Insights

Human initiator caspases-8 and -10 induce apoptosis in yeast, causing cell death and various cellular alterations. Caspase-10 expression also disrupts DNA replication checkpoints and resembles autophagy.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Biochemistry

Background:

  • Caspases are key proteases in apoptosis, but their regulation and substrates require further study.
  • Understanding caspase function in a heterologous system can elucidate conserved mechanisms.

Purpose of the Study:

  • To investigate the effects of human initiator caspases-8 and -10 expression in Saccharomyces cerevisiae.
  • To explore caspase-mediated cellular alterations and their dependence on yeast apoptotic machinery.

Main Methods:

  • Ectopic expression of human CASP8 and CASP10 in yeast.
  • Analysis of apoptotic markers: reactive oxygen species (ROS) production, chromatin condensation, and phosphatidylserine externalization.
  • Assessment of DNA replication, cell cycle checkpoints, vacuolization, autophagy, cytoskeleton, cell wall, and endoplasmic reticulum integrity.

Main Results:

  • Expression of CASP10 and CASP8 induced significant apoptotic markers and cell death in yeast.
  • Caspase-10 expression led to DNA replication escape from the intra-S checkpoint and induced vacuolization resembling autophagy.
  • Intracellular damage included actin cytoskeleton disorganization, cell wall defects, and endoplasmic reticulum lumen aberrations.
  • Caspase-induced cell death required proteolytic activation but was independent of yeast proteins Aif1 and Mca1, and mitochondria.

Conclusions:

  • Human initiator caspases can trigger apoptosis and diverse cellular dysfunctions in yeast.
  • Caspase-10 exhibits unique effects on yeast cell cycle regulation and autophagy-like processes.
  • Yeast serves as a valuable model for studying conserved aspects of caspase-induced cell death and cellular damage.

More Related Videos

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila13:21

In Vivo Biosensor Tracks Non-apoptotic Caspase Activity in Drosophila

Published on: November 27, 2016

Saccharomyces cerevisiae Models of Alzheimer's Disease to Screen Genes, Mutations, and Chemicals Affecting Amyloid Beta Production by γ-Secretase11:57

Saccharomyces cerevisiae Models of Alzheimer's Disease to Screen Genes, Mutations, and Chemicals Affecting Amyloid Beta Production by γ-Secretase

Published on: June 24, 2025

Related Concept Videos

Caspases01:24

Caspases

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 cells.
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 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...
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 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...
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...