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Arginyltransferase1 drives a mitochondria-dependent program to induce cell death.

Akhilesh Kumar1,2, Corin R O'Shea3, Vikas K Yadav2

  • 1Department of Molecular & Cellular Pharmacology, University of Miami Miller School of Medicine, Miami, FL, USA.

Biorxiv : the Preprint Server for Biology
|November 28, 2024
PubMed
Summary

Arginyltransferase1 (Ate1) enzyme regulates cell death by translocating to mitochondria under oxidative stress. This mitochondrial localization is crucial for apoptosis, independent of cytosolic protein degradation pathways.

Keywords:
ArginylationAte1apoptosisarginyltransferasemitochondrialposttranslational modificationprogrammed cell deathubiquitination

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Area of Science:

  • Cell Biology
  • Biochemistry
  • Molecular Biology

Background:

  • Cell death regulation is vital for stress adaptation and signaling.
  • Arginyltransferase1 (Ate1) is an evolutionarily conserved enzyme involved in eukaryotic cell death.
  • Previous research focused on Ate1's cytosolic role in protein degradation, overlooking its role in cell death.

Purpose of the Study:

  • To investigate the role of arginyltransferase1 (Ate1) in cell death.
  • To determine the subcellular localization and function of Ate1 under oxidative stress.
  • To elucidate the mechanism of Ate1-induced cell death.

Main Methods:

  • Utilized budding yeast as a model organism.
  • Investigated Ate1 localization under oxidative stress conditions.
  • Analyzed Ate1-induced cell death pathways, including mitochondrial involvement and cytosolic degradation pathways.

Main Results:

  • Mitochondrial translocation of Ate1 is induced by oxidative stressors and is essential for apoptosis.
  • Ate1-induced cell death depends on mitochondrial permeability pore formation and mitochondrial factors, but not directly on ROS or ETC activity.
  • Cytosolic protein degradation pathways (ubiquitin-proteasome, autophagy, ER stress) do not significantly impact Ate1-induced cell death.

Conclusions:

  • Arginyltransferase1 (Ate1) controls a mitochondria-dependent cell death pathway.
  • Mitochondrial localization of Ate1 is a key event in stress-induced apoptosis.
  • Ate1's role in cell death is primarily mitochondrial, distinct from its known cytosolic functions.