Mitochondrial Release of Apoptosis-inducing Factor Occurs Downstream of Cytochrome C Release in Response to Several Proapoptotic Stimuli

Overview

Journal J Cell Biol

Specialty Cell Biology

Date 2002 Dec 18

PMID 12486111

Citations 92

Authors

Damien Arnoult

Philippe Parone

Jean-Claude Martinou

Bruno Antonsson

Jerome Estaquier

Jean Claude Ameisen

Affiliations

Soon will be listed here.

Abstract

Mitochondrial outer membrane permeabilization by proapoptotic Bcl-2 family proteins, such as Bax, plays a crucial role in apoptosis induction. However, whether this only causes the intracytosolic release of inducers of caspase-dependent death, such as cytochrome c, or also of caspase-independent death, such as apoptosis-inducing factor (AIF) remains unknown. Here, we show that on isolated mitochondria, Bax causes the release of cytochrome c, but not of AIF, and the association of AIF with the mitochondrial inner membrane provides a simple explanation for its lack of release upon Bax-mediated outer membrane permeabilization. In cells overexpressing Bax or treated either with the Bax- or Bak-dependent proapoptotic drugs staurosporine or actinomycin D, or with hydrogen peroxide, caspase inhibitors did not affect the intracytosolic translocation of cytochrome c, but prevented that of AIF. These results provide a paradigm for mitochondria-dependent death pathways in which AIF cannot substitute for caspase executioners because its intracytosolic release occurs downstream of that of cytochrome c.

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