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Detection of Mitochondria Membrane Potential to Study CLIC4 Knockdown-induced HN4 Cell Apoptosis In Vitro
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Cardiolipin or MTCH2 can serve as tBID receptors during apoptosis

E Raemy1, S Montessuit1, S Pierredon1

  • 1Department of Cell Biology, University of Geneva, Quai Ernest-Ansermet 30, 1211 Geneva 4, Switzerland.

Cell Death and Differentiation
|January 23, 2016
PubMed

Insights

Cardiolipin (CL) and MTCH2 are not essential for apoptosis initiation by tBID in HCT116 cells. However, both CL and MTCH2 play redundant roles in tBID recruitment to mitochondria during apoptosis.

Area of Science:

  • Cellular biology
  • Biochemistry
  • Molecular biology

Background:

  • Apoptosis involves mitochondrial outer membrane permeabilization (MOM) triggered by BAX and BAK.
  • BH3-only proteins like tBID and mitochondrial lipids are implicated in BAX/BAK activation.
  • Cardiolipin (CL) enhances tBID-induced BAX activation in vitro, but its in vivo role is unclear.

Purpose of the Study:

  • To investigate the necessity of cardiolipin (CL) and MTCH2 in tBID-induced BAX activation and apoptosis.
  • To determine the roles of CL and MTCH2 in tBID recruitment to the mitochondrial outer membrane (MOM).

Main Methods:

  • Generated CL-deficient human HCT116 cells using homologous recombination.
  • Assessed cell viability, oxidative phosphorylation, and apoptosis induction.
  • Examined tBID recruitment to mitochondria upon MTCH2 or CL depletion.

Main Results:

  • CL-deficient cells were viable but had impaired oxidative phosphorylation and galactose growth.
  • CL absence did not prevent tBID-induced BAX activation or TRAIL-induced apoptosis.
  • MTCH2 downregulation alone did not inhibit tBID mitochondrial recruitment.
  • Combined depletion of CL and MTCH2 significantly reduced tBID recruitment.

Conclusions:

  • Cardiolipin is not essential for tBID-mediated apoptosis initiation in HCT116 cells.
  • CL and MTCH2 exhibit redundant functions in mediating tBID recruitment to the MOM in these cells.

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