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STX17 dynamically regulated by Fis1 induces mitophagy via hierarchical macroautophagic mechanism

Hongxu Xian1, Qiaoyun Yang1, Lin Xiao1

  • 1Department of Biological Sciences, Faculty of Science, National University of Singapore, 14 Science Drive 4, 117543, Singapore, Singapore.

Nature Communications
|May 5, 2019
PubMed

Insights

Scientists discovered a new mitophagy pathway independent of PINK1/Parkin. Syntaxin 17 (STX17) initiates this process when Fis1 is depleted, regulating mitochondrial quality control.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Autophagy Research

Background:

  • Mitophagy, the selective removal of damaged mitochondria, is crucial for cellular health.
  • While the PINK1/Parkin-dependent pathway is understood, PINK1/Parkin-independent mitophagy remains largely uncharacterized.
  • Mitochondrial quality control is essential for preventing disease associated with mitochondrial dysfunction.

Purpose of the Study:

  • To elucidate a novel PINK1/Parkin-independent mitophagy pathway.
  • To investigate the role of Syntaxin 17 (STX17) and Fis1 in mitophagy.
  • To understand the molecular mechanisms regulating mitochondrial turnover.

Main Methods:

  • Super-resolution structured illumination microscopy (SR-SIM) to visualize protein dynamics.
  • Proteomics analysis to identify protein interactions.
  • Functional assays to assess mitophagy and mitochondrial respiration.

Main Results:

  • Syntaxin 17 (STX17) initiates mitophagy upon Fis1 depletion, independent of PINK1/Parkin.
  • Fis1 regulates STX17 localization between the ER and mitochondria; its loss causes STX17 accumulation on mitochondria.
  • STX17 self-oligomerization and interaction with ATG14 trigger mitophagosome formation and lysosomal fusion, linking macroautophagy to mitochondrial turnover.

Conclusions:

  • A novel PINK1/Parkin-independent mitophagy pathway regulated by Fis1 and STX17 has been identified.
  • Fis1 acts as a key regulator of mitochondrial quality control by modulating STX17 function.
  • This discovery provides new insights into the mechanisms of mitochondrial turnover and cellular homeostasis.

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