Temporal dissection of Bax-induced events leading to fission of the single mitochondrion in Trypanosoma brucei

EMBO Rep. 2004 Mar;5(3):268-73. doi: 10.1038/sj.embor.7400095. Epub 2004 Feb 13.

Abstract

The protozoan Trypanosoma brucei has a single mitochondrion and lacks an apoptotic machinery. Here we show that expression of the proapoptotic protein Bax in T. brucei causes the release of cytochrome c, the depolarization of the mitochondrial membrane potential and mitochondrial fission. However, in contrast to mammalian cells, the three events are temporally well separated. The release of cytochrome c from the intermembrane space precedes mitochondrial fission, showing that it does not depend on mitochondrial fragmentation. Furthermore, halting Bax expression allows some cells to recover even after mitochondrial fission, the last recorded event, went to completion, indicating that all three Bax-induced events are, in principle, reversible.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis
  • Cell Line
  • Chaperonin 60 / metabolism
  • Cytochromes c / metabolism
  • DNA, Complementary / genetics
  • Fluorescent Antibody Technique
  • Gene Expression
  • Gene Expression Regulation
  • Humans
  • Membrane Potentials
  • Mitochondria / metabolism
  • Mitochondria / ultrastructure*
  • Proto-Oncogene Proteins c-bcl-2 / genetics
  • Proto-Oncogene Proteins c-bcl-2 / metabolism*
  • Tetracycline / metabolism
  • Transformation, Genetic
  • Trypanosoma brucei brucei / physiology
  • Trypanosoma brucei brucei / ultrastructure*
  • bcl-2-Associated X Protein
  • bcl-X Protein

Substances

  • BAX protein, human
  • BCL2L1 protein, human
  • Chaperonin 60
  • DNA, Complementary
  • Proto-Oncogene Proteins c-bcl-2
  • bcl-2-Associated X Protein
  • bcl-X Protein
  • Cytochromes c
  • Tetracycline