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Miro1 expression alters global gene expression, ERK1/2 phosphorylation, oxidation and cell cycle progression

Nathaniel Shannon1, Cory Raymond1, Chloe Palmer1

  • 1Department of Pathology and Laboratory Medicine, University of Vermont Cancer Center, Larner College of Medicine, Burlington, VT 05405, USA.

Journal of Cell Science
|March 11, 2025
PubMed

Insights

Mitochondrial protein Miro1 deletion causes slower cell growth and cell cycle defects in mouse cells. This is linked to altered MAPK signaling and ERK1/2 oxidation, highlighting Miro1

Area of Science:

  • Cell Biology
  • Mitochondrial Dynamics
  • Molecular Signaling

Background:

  • Mitochondrial positioning is crucial for cellular energy and signaling.
  • Miro1 facilitates mitochondria attachment to motor proteins for transport.
  • Loss of Miro1 in MEFs causes mitochondrial perinuclear sequestration and disrupted signaling.

Purpose of the Study:

  • Investigate the impact of Miro1 deletion on MEF cell cycle and proliferation.
  • Identify transcriptional changes associated with Miro1 expression.
  • Elucidate the role of Miro1 in regulating MAPK signaling pathways, specifically ERK1/2.

Main Methods:

  • Miro1 knockout (Miro1-/-) and re-expression in mouse embryonic fibroblasts (MEFs).
  • Cell cycle analysis (G1 and S phase distribution).
  • RNA sequencing to identify differentially expressed genes.
  • Western blotting to assess protein phosphorylation and oxidation states.

Main Results:

  • Miro1-/- MEFs exhibit slower growth and cell cycle arrest (decreased G1, increased S phase).
  • RNA sequencing revealed altered gene expression in MAPK signaling, proliferation, and migration pathways.
  • Elevated ERK1/2 phosphorylation and increased oxidation were observed in Miro1-/- MEFs.
  • DUSP1-DUSP6 expression and oxidation levels remained unchanged.

Conclusions:

  • Miro1 deletion impacts cell cycle progression and proliferation.
  • Transcriptional changes and altered ERK1/2 regulation are consequences of Miro1 loss.
  • Miro1 plays a significant role in maintaining mitochondrial positioning and cellular homeostasis.
Keywords:
Cell cycleERK1/2Miro1MitochondriaRedox

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