Light-activated mitochondrial fission through optogenetic control of mitochondria-lysosome contacts

Kangqiang Qiu1, Weiwei Zou2, Hongbao Fang1

  • 1Department of Cancer Biology, University of Cincinnati College of Medicine, Cincinnati, OH, 45267, USA.

Nature Communications
|July 25, 2022
PubMed

Insights

Researchers developed optogenetic control of mitochondria-lysosome contacts to induce mitochondrial fission. This method aids in studying mitochondrial dynamics and offers potential for treating mitochondrial diseases.

Area of Science:

  • Cell Biology
  • Mitochondrial Biology
  • Optogenetics

Background:

  • Mitochondria are dynamic organelles essential for cellular homeostasis.
  • Mitochondrial fission, the fragmentation of mitochondria, is crucial for maintaining mitochondrial function and cellular health.
  • Defects in mitochondrial fission are linked to various mitochondrial diseases.

Purpose of the Study:

  • To develop a spatiotemporally accurate method for inducing mitochondrial fission.
  • To investigate the role of mitochondria-lysosome contacts (MLCs) in regulating mitochondrial fission.
  • To explore the therapeutic potential of optogenetically controlled mitochondrial fission for mitochondrial diseases.

Main Methods:

  • Utilized optogenetics to control mitochondria-lysosome contacts (MLCs) via blue-light-induced photoactivatable dimerizers.
  • Developed a system for real-time optogenetic induction and tracking of mitochondrial fission in living cells.
  • Assessed mitochondrial function in SLC25A46-/- cells with induced mitochondrial fission.

Main Results:

  • Successfully induced mitochondrial fission with spatiotemporal precision using optogenetic control of MLCs.
  • Established a method to measure mitochondrial fission rates in real-time.
  • Demonstrated partial restoration of mitochondrial function in SLC25A46-/- cells with defective fission.

Conclusions:

  • Optogenetic control of MLCs provides a powerful tool for studying mitochondrial fission.
  • This system offers a potential platform for developing new therapeutic strategies for mitochondrial diseases characterized by fission defects.