Related Experiment Video

Updated: Aug 13, 2026

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c
07:42

Activation of Apoptosis by Cytoplasmic Microinjection of Cytochrome c

Published on: June 29, 2011

Bax and Bcl-xL independently regulate apoptotic changes of yeast mitochondria that require VDAC but not adenine

S Shimizu1, Y Shinohara, Y Tsujimoto

  • 1Department of Medical Genetics, Osaka University Graduate School of Medicine, Biomedical Research Center, 2-2 Yamadaoka, Suita, Osaka 565-0871, Japan.

Oncogene
|September 12, 2000
PubMed

Insights

Mitochondria

Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Mitochondria are key regulators of apoptosis, releasing molecules like cytochrome c.
  • Bcl-2 family proteins control these apoptotic events.
  • The roles of voltage-dependent anion channel (VDAC) and adenine nucleotide translocator (ANT) in mitochondrial apoptosis are debated.

Purpose of the Study:

  • To investigate the specific roles of ANT and VDAC in mitochondrial changes induced by Bax and permeability transition (PT).
  • To clarify the interaction of Bax and Bcl-xL with ANT and VDAC during apoptosis.

Main Methods:

  • Experiments were conducted on isolated rat and yeast mitochondria.
  • Yeast strains deficient in VDAC or ANT were utilized.
  • Mitochondrial functions like ADP/ATP exchange, cytochrome c release, membrane potential loss, and swelling were measured.
  • Bax- and PT-induced changes were assessed in wild-type and mutant yeast cells.

Main Results:

  • Bax did not impact ANT's ADP/ATP exchange activity in rat or yeast mitochondria.
  • VDAC-deficient yeast mitochondria resisted Bax- and PT-induced cytochrome c release, membrane potential loss, and swelling.
  • ANT-deficient yeast mitochondria did not show this resistance.
  • Bcl-xL inhibited these changes in both ANT-deficient and wild-type yeast mitochondria.
  • Bax induced cytochrome c release in wild-type yeast but not VDAC1-deficient yeast cells.

Conclusions:

  • VDAC, not ANT, is essential for Bax- and PT-induced apoptotic mitochondrial changes.
  • Bcl-xL and Bax can regulate mitochondrial membrane permeability independently of other Bcl-2 family members.

More Related Videos

Examining BCL-2 Family Function with Large Unilamellar Vesicles08:35

Examining BCL-2 Family Function with Large Unilamellar Vesicles

Published on: October 5, 2012

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling08:51

Applying an Inducible Expression System to Study Interference of Bacterial Virulence Factors with Intracellular Signaling

Published on: June 25, 2015

Related Concept Videos

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...
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...
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...
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...