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Myo19 tethers mitochondria to endoplasmic reticulum-associated actin to promote mitochondrial fission

Stephen M Coscia1,2,3, Cameron P Thompson1,3,4, Qing Tang1,3

  • 1Department of Physiology, University of Pennsylvania Perelman School of Medicine, Philadelphia, PA 19104, USA.

Journal of Cell Science
|February 6, 2023
PubMed

Insights

Myosin 19 (Myo19) is crucial for mitochondrial fission, acting as an actin tether that stabilizes mitochondria-ER contacts. This interaction promotes the fragmentation of mitochondria, essential for cellular health.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Mitochondrial Dynamics

Background:

  • Mitochondrial homeostasis relies on a balance between fission and fusion.
  • The actin cytoskeleton plays a role in mitochondrial fission.

Purpose of the Study:

  • To investigate the role of myosin 19 (Myo19) in mitochondrial fission.
  • To elucidate the mechanism by which Myo19 regulates mitochondrial morphology.

Main Methods:

  • Myo19 knockdown and overexpression in cells.
  • Analysis of mitochondrial morphology using microscopy.
  • Site-directed mutagenesis of Myo19.
  • Super-resolution imaging.
  • Depletion of INF2 and Spire1C.
  • Split-luciferase assay to assess mitochondria-ER contacts.

Main Results:

  • Myo19 knockdown led to mitochondrial elongation; overexpression caused fragmentation.
  • Myo19's ATPase activity and actin-binding are essential for fragmentation.
  • Myo19 localizes to mitochondria via metaxins.
  • Myo19-driven fragmentation depends on INF2 and Spire1C.
  • Myo19 stabilizes mitochondria-ER contacts, which are reduced upon Myo19 depletion.

Conclusions:

  • Myo19 acts as a dynamic actin-binding tether facilitating mitochondrial fragmentation.
  • Myo19 promotes fission by stabilizing mitochondria-ER contacts through interaction with ER-associated actin.
Keywords:
ActinEndoplasmic reticulumFissionMitochondriaMyo19

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