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APC binds the Miro/Milton motor complex to stimulate transport of mitochondria to the plasma membrane

Kate M Mills1, Mariana G Brocardo2, Beric R Henderson2

  • 1Centre for Cancer Research, Westmead Institute for Medical Research, University of Sydney, Westmead, NSW 2145, Australia.

Molecular Biology of the Cell
|December 15, 2015
PubMed

Insights

Adenomatous polyposis coli (APC) protein is crucial for mitochondrial transport. Loss of APC disrupts mitochondria distribution, impacting cellular energy supply and potentially contributing to cancer progression.

Area of Science:

  • Cell Biology
  • Molecular Biology
  • Cancer Research

Background:

  • Adenomatous polyposis coli (APC) is a tumor suppressor gene involved in Wnt signaling, mitosis, and cytoskeleton regulation.
  • Dysfunctional APC is linked to various cancers, particularly colorectal cancer.
  • The precise roles of APC in cellular processes beyond its known functions are still being investigated.

Purpose of the Study:

  • To investigate a novel role for APC in mitochondrial transport.
  • To identify the molecular mechanisms underlying APC's involvement in mitochondria dynamics.
  • To explore the implications of APC-mediated mitochondrial transport in cancer.

Main Methods:

  • Small interfering RNA (siRNA) to silence wild-type APC expression.
  • Identification of APC protein interactions using co-immunoprecipitation and yeast two-hybrid assays.
  • Proximity ligation assays to detect endogenous APC-Miro/Milton complexes.
  • Live-cell imaging to analyze mitochondrial transport dynamics.
  • Reconstitution of wild-type APC in cancer cells.

Main Results:

  • Silencing APC led to perinuclear redistribution of mitochondria.
  • APC interacts with the Miro/Milton mitochondrial kinesin-motor complex via its C-terminus.
  • Truncating APC mutations disrupted Miro/Milton binding and complex formation, affecting mitochondrial distribution.
  • Loss of APC impaired anterograde mitochondrial transport frequency to the cell membrane.
  • Restoration of wild-type APC rescued mitochondrial distribution defects.

Conclusions:

  • APC plays a significant role in regulating mitochondrial transport to the cell periphery.
  • APC facilitates mitochondrial transport by interacting with the Miro/Milton complex.
  • Disruption of APC-mediated mitochondrial transport may impair energy supply for cellular functions like migration, contributing to cancer development.

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