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MicroRNA-338 regulates the axonal expression of multiple nuclear-encoded mitochondrial mRNAs encoding subunits of the

Armaz Aschrafi1, Amar N Kar, Orlangie Natera-Naranjo

  • 1Laboratory of Molecular Biology, National Institute of Mental Health, National Institutes of Health, Bethesda, MD, 20892-1381, USA.

Cellular and Molecular Life Sciences : CMLS
|July 10, 2012
PubMed

Insights

Brain-specific microRNA-338 (miR-338) coordinates the expression of mitochondrial genes in axons. This regulation impacts axonal reactive oxygen species levels and growth, suggesting a role in local energy metabolism.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • MicroRNAs (miRNAs) are small, non-coding RNAs regulating gene expression post-transcriptionally.
  • These molecules can coordinate the regulation of multiple genes involved in related cellular functions.
  • Brain-specific miR-338 was previously shown to modulate axonal expression of cytochrome c oxidase IV (COXIV).

Purpose of the Study:

  • To investigate if miR-338 also regulates ATP synthase (ATP5G1) expression in axons.
  • To determine the effect of miR-338 on axonal energy metabolism and growth.
  • To elucidate the mechanism of miR-338-mediated coordinate regulation of mitochondrial gene expression.

Main Methods:

  • Bioinformatic analysis to identify putative miR-338 binding sites.
  • Modulation of miR-338 levels in axons.
  • Quantitative analysis of COXIV and ATP5G1 mRNA and protein expression.
  • Measurement of axonal reactive oxygen species (ROS) levels.
  • Assessment of axonal growth.

Main Results:

  • ATP synthase (ATP5G1) mRNA was identified as containing a putative miR-338 binding site.
  • Modulating miR-338 levels in axons altered both COXIV and ATP5G1 expression.
  • miR-338 modulation significantly affected axonal ROS levels and axonal growth.

Conclusions:

  • miR-338 coordinates the expression of multiple nuclear-encoded mitochondrial mRNAs, including COXIV and ATP5G1, within the axon.
  • This coordinate regulation by miR-338 impacts local axonal energy metabolism, ROS production, and axonal growth.
  • Findings reveal a novel mechanism for miR-338 in regulating axonal function via mitochondrial gene expression.

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