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Post-translational decrease in respiratory chain proteins in the Polg mutator mouse brain.

David N Hauser1, Allissa A Dillman2, Jinhui Ding3

  • 1Cell Biology and Gene Expression Section, Laboratory of Neurogenetics, National Institute on Aging, National Institutes of Health, Bethesda, Maryland, United States of America; Brown University/National Institutes of Health Graduate Partnership Program, Department of Neuroscience, Brown University, Providence, Rhode Island, United States of America.

Plos One
|April 12, 2014
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Summary
This summary is machine-generated.

Mitochondrial DNA damage from polymerase gamma (Polg) mutations accelerates aging. Polg mutator mice show decreased mitochondrial proteins, not due to mRNA changes, indicating post-translational effects on aging.

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Area of Science:

  • Molecular Biology
  • Aging Research
  • Mitochondrial Biology

Background:

  • Mitochondrial DNA (mtDNA) damage is implicated in aging.
  • Mice with inactivating mutations in polymerase gamma (Polg) exhibit a progeroid (premature aging) phenotype.
  • Understanding the molecular basis of this phenotype is crucial for aging research.

Purpose of the Study:

  • To investigate the molecular mechanisms underlying the progeroid phenotype in Polg mutator mice.
  • To compare protein and mRNA abundance in the brains of Polg mutator mice and control animals.
  • To identify specific molecular changes associated with mtDNA damage and aging.

Main Methods:

  • Utilized iTRAQ (isobaric tags for relative and absolute quantitation) for proteomic analysis.
  • Employed RNA-Seq (RNA sequencing) for transcriptomic analysis.
  • Compared protein and mRNA levels in the brains of one-year-old Polg mutator mice and age-matched controls.

Main Results:

  • A specific decrease in mitochondrial respiratory chain proteins was observed in Polg mutator mouse brains.
  • Several nuclear-encoded mitochondrial components were also found to be decreased in abundance.
  • No correlation was found between observed protein level changes and mRNA expression levels.

Conclusions:

  • Mutations in Polg lead to post-translational modifications affecting mitochondrial protein abundance.
  • The observed decrease in mitochondrial proteins is not a direct result of altered mRNA expression.
  • These findings highlight the role of post-translational regulation in mtDNA damage-induced aging.