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NDUFV2 pseudogene (NDUFV2P1) contributes to mitochondrial complex I deficits in schizophrenia

Oded Bergman1, Rachel Karry1, Jumana Milhem1

  • 1Laboratory of Psychobiology, Department of Psychiatry, Rambam Health Care Campus, B. Rappaport Faculty of Medicine and Rappaport Family Institute for Research in Medical Sciences, Technion-Israel Institute of Technology, Haifa, Israel.

Molecular Psychiatry
|December 12, 2018
PubMed

Insights

Mitochondrial complex I dysfunction in schizophrenia may involve the NDUFV2 pseudogene (NDUFV2P1). Increased NDUFV2P1 expression inversely correlates with NDUFV2 protein levels and cellular respiration, suggesting a novel regulatory role.

Area of Science:

  • Neuroscience
  • Cell Biology
  • Genetics

Background:

  • Mitochondrial dysfunction, particularly Complex I (CoI) deficits, is implicated in schizophrenia.
  • Cellular crosstalk between mitochondria and other components regulates gene expression.

Purpose of the Study:

  • To investigate the role of mitochondrial CoI dysfunction in schizophrenia.
  • To explore the specific involvement of the NDUFV2 gene and its pseudogene (NDUFV2P1) in schizophrenia-related cellular changes.

Main Methods:

  • Analysis of CoI activity and NDUFV2 protein/mRNA levels in schizophrenia-derived cell lines.
  • Quantification of NDUFV2 pseudogene (NDUFV2P1) expression in cell lines and postmortem brain specimens.
  • Correlation analysis between NDUFV2P1 levels, NDUFV2 protein, and cellular respiration.

Main Results:

  • Schizophrenia-derived cells exhibit deficits in CoI activity and NDUFV2 protein levels without changes in mRNA.
  • NDUFV2P1 expression is elevated in schizophrenia cells and brain tissue.
  • NDUFV2P1 levels inversely correlate with NDUFV2 protein and CoI-driven respiration.

Conclusions:

  • Pseudogene dysregulation, specifically NDUFV2P1, may contribute to CoI dysfunction in schizophrenia.
  • This pseudogene-parent gene interaction could be part of a feedback loop exacerbating mitochondrial dysfunction.
  • Abnormal pseudogene expression might influence genome-wide gene regulation in schizophrenia.

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