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Drosophila Omi, a mitochondrial-localized IAP antagonist and proapoptotic serine protease

Madhavi Challa1, Srinivas Malladi, Brett J Pellock

  • 1Division of Pharmacology and Toxicology, College of Pharmacy, The University of Texas at Austin, Austin, TX, USA.

The EMBO Journal
|June 9, 2007
PubMed

Insights

In flies, Drosophila Omi (dOmi) is released from mitochondria during apoptosis, degrading inhibitors of apoptosis proteins (IAPs) and triggering cell death. This study clarifies dOmi

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Developmental Biology

Background:

  • The role of mitochondrial outer membrane permeabilization in apoptosis is debated in flies.
  • Drosophila Omi (dOmi), a homolog of mammalian Omi/HtrA2, is a mitochondrial intermembrane space protein.

Purpose of the Study:

  • To investigate the function of Drosophila Omi (dOmi) in fly apoptosis.
  • To determine if mitochondrial outer membrane permeabilization occurs and releases proapoptotic factors in flies.

Main Methods:

  • Demonstrated dOmi localization and processing within mitochondria.
  • Analyzed dOmi release into the cytosol upon apoptotic stimuli.
  • Investigated dOmi's interaction with Drosophila IAP1 (DIAP1) and caspases.
  • Assessed dOmi's role in apoptosis induction in cell culture and fly eyes.

Main Results:

  • dOmi is a developmentally regulated mitochondrial intermembrane space protein.
  • Mature dOmi is released into the cytosol and binds to DIAP1, displacing initiator caspase DRONC.
  • dOmi degrades DIAP1, overcoming its caspase inhibition.
  • dOmi induces apoptosis in cultured cells and the developing fly eye.

Conclusions:

  • Mitochondrial outer membrane permeabilization occurs during apoptosis in flies.
  • dOmi is a bona fide proapoptotic protein released from mitochondria in flies.
  • dOmi plays a crucial role in regulating apoptosis by degrading IAPs.

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