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Trinucleotide repeat instability via DNA base excision repair.

Yanhao Lai1, Jill M Beaver2, Eduardo Laverde2

  • 1Department of Chemistry and Biochemistry, Florida International University, 11200 SW 8th Street, Miami, FL, 33199, United States; Biomolecular Sciences Institute, Florida International University, 11200 SW 8th Street, Miami, FL, 33199, United States.

DNA Repair
|October 22, 2020
PubMed
Summary

DNA base excision repair (BER) actively regulates trinucleotide repeat (TNR) instability, a key factor in neurodegenerative diseases and cancer. Understanding BER

Keywords:
DNA base damageDNA base excision repairDNA repair crosstalkTrinucleotide repeat instability

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Area of Science:

  • Molecular Biology
  • Genetics
  • Genomics

Background:

  • Trinucleotide repeat (TNR) instability underlies over 40 human diseases, including neurodegenerative disorders and cancers.
  • Somatic TNR instability is influenced by DNA replication, repair, recombination, and transcription.
  • DNA base damage and the base excision repair (BER) pathway are increasingly recognized as critical regulators of TNR instability.

Purpose of the Study:

  • To review recent advances in understanding the molecular mechanisms of BER-mediated TNR instability.
  • To explore the interplay between DNA base lesions, BER, and non-B DNA structures in TNR instability.
  • To discuss the role of BER enzyme coordination and crosstalk with DNA mismatch repair (MMR) in TNR expansion.

Main Methods:

  • Review of current literature on BER pathways and TNR instability.
  • Analysis of molecular mechanisms linking DNA base damage and repair to repeat dynamics.
  • Discussion of experimental evidence for BER-mediated regulation of somatic TNR instability.

Main Results:

  • BER pathway components and DNA base lesions within TNRs are key determinants of repeat instability.
  • The balance between removal and addition of TNRs is modulated by BER enzyme activity.
  • Crosstalk between BER and MMR can lead to TNR expansion, contributing to disease pathogenesis.

Conclusions:

  • BER plays a crucial role in regulating somatic TNR instability through coordinated enzyme activity and crosstalk with MMR.
  • Targeting BER pathways may offer novel therapeutic strategies for TNR-related diseases.
  • Further research into BER-mediated TNR instability is essential for disease prevention and treatment.