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Taming an Ancient Guest: Autophagy in Mitochondrial Quality Control

Angelina Gross (ORCID: 0000-0002-8096-0831)
  • Grant DOI 10.55776/PAT2651925
  • Funding program Principal Investigator Projects
  • Status ongoing
  • Start January 1, 2026
  • End December 31, 2029
  • Funding amount € 449,869

Disciplines

Biology (100%)

Keywords

  • Selective autophagy,
  • Mitochondria,
  • Stress response,
  • Cellular homeostasis,
  • Plant fitness
Abstract

Cells - whether from fungi, plants, or humans - organize their functions in highly specialized compartments called organelles. Mitochondria, for example, are organelles that meet the cellular energy demand and build key molecular building blocks. Interestingly, mitochondria were once bacteria, taken up and domesticated by our unicellular ancestors. This ancient partnership works, because quality-control mechanisms evolved, that keep mitochondria functional and prevent harmful effects on the cell. A central aspect of this quality control is the regulation of molecular communication between mitochondria and the rest of the cell. This communication occurs for example through specialized pores in the outer mitochondrial membrane allowing the exchange of molecules. Beyond the transport function, these pores act as signaling and coordination channels. In this project, we ask how cells adjust the quality and quantity of these pores to regulate molecular traffic and maintain cellular homeostasis. Autophagy is the cells central recycling system: it recognizes damaged or superfluous material and degrades it. Our preliminary data indicate that autophagy plays a major role in turning over and recycling mitochondrial pores. We will identify which components of the autophagy machinery detect and remove excess or non-functional pores and determine how this process shapes communication between mitochondria and the cell. We use budding yeast Saccharomyces cerevisiae, an established model for elucidating fundamental molecular mechanisms, to identify the genetic components of autophagy-mediated pore degradation. We then transfer this knowledge to the plant model Arabidopsis thaliana and test how impaired pore degradation affects plant stress resistance and survival. This combined approach delivers insights from single molecules to multicellular organisms. In the long term, we contribute to understanding how cells communicate with their mitochondria, laying foundations with relevance from plant breeding to medicine.

Research institution(s)
  • Universität für Bodenkultur Wien - 100%
Project participants
  • Yasin Dagdas, Ruprecht-Karls-Universität Heidelberg , national collaboration partner
International project participants
  • Yasin Dagdas, Ruprecht-Karls-Universität Heidelberg - Germany

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