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RAD52 is required for RNA-templated recombination repair in post-mitotic neurons.

Starr Welty1,2, Yaqun Teng1,2,3, Zhuobin Liang4

  • 1From the Department of Microbiology and Molecular Genetics, University of Pittsburgh School of Medicine, Pittsburgh, Pennsylvania 15219.

The Journal of Biological Chemistry
|December 9, 2017
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Summary

Post-mitotic neurons use an RNA-tempted homologous recombination (HR) pathway to repair DNA double-strand breaks (DSBs). Amyloid beta disrupts this repair, potentially causing neurodegeneration in Alzheimer's disease.

Keywords:
Alzheimer's diseaseRNAamyloid β (Aβ)neuronoxidative damagerecombination

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Genetics

Background:

  • Post-mitotic neurons were thought to only use error-prone DNA repair pathways.
  • Previous research indicated active transcription can trigger DNA repair in non-replicating cells.

Purpose of the Study:

  • To investigate the DNA repair mechanisms in terminally differentiated neurons.
  • To determine if homologous recombination (HR) is active in post-mitotic neurons.
  • To explore the role of RNA in neuronal DNA repair.

Main Methods:

  • Observed the recruitment of RAD52 protein to DNA double-strand break (DSB) sites in neurons.
  • Investigated the dependence of RAD52 recruitment on active transcription and nascent mRNA.
  • Assessed the impact of transcription inhibition on RAD52 recruitment.
  • Examined the effect of amyloid beta on RAD52 expression and DNA damage response.

Main Results:

  • RAD52, an HR repair protein, is recruited to DSBs in post-mitotic neurons.
  • RAD52 recruitment is dependent on nascent mRNA from active transcription, indicating an RNA-templated HR repair mechanism.
  • Transcription inhibition reduces RAD52 recruitment.
  • Amyloid beta inhibits RAD52 expression and DNA damage response.

Conclusions:

  • Post-mitotic neurons possess an RNA-dependent homologous recombination (HR) DNA repair pathway.
  • This novel repair mechanism is crucial for maintaining neuronal genomic stability.
  • Impaired RNA-templated HR repair due to factors like amyloid beta may contribute to neurodegenerative diseases such as Alzheimer's disease.