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Mre11-Sae2 and RPA Collaborate to Prevent Palindromic Gene Amplification

Sarah K Deng1, Yi Yin2, Thomas D Petes2

  • 1Department of Microbiology & Immunology, Columbia University Medical Center, New York, NY 10032, USA.

Molecular Cell
|November 7, 2015
PubMed

Insights

Small inverted repeats drive palindromic duplications, a key cancer mechanism. RPA dysfunction dramatically increases these rearrangements by promoting hairpin formation and replication errors.

Area of Science:

  • Genetics
  • Molecular Biology
  • Cancer Research

Background:

  • Palindromic gene amplification is observed in cancer cells.
  • Foldback priming at DNA double-stranded breaks is a proposed mechanism for this amplification.

Purpose of the Study:

  • To investigate the role of small inverted repeats in driving palindromic duplications.
  • To elucidate the mechanisms underlying chromosomal rearrangements in cells deficient in DNA repair factors.

Main Methods:

  • Analysis of chromosomal rearrangements in yeast cells lacking Sae2 or Mre11 nuclease.
  • Assessment of the impact of RPA (Replication Protein A) dysfunction on palindromic duplication frequency.

Main Results:

  • Small (5-9 bp) inverted repeats were found to drive the formation of large palindromic duplications.
  • RPA dysfunction increased palindromic duplications by approximately 1,000-fold in Sae2 or Mre11-deficient cells.
  • Dicentric isochromosomes formed via hairpin-capped chromosome replication and subsequent repair involving dispersed repeats and telomeres.

Conclusions:

  • Secondary structures in single-stranded DNA are significant instigators of genome instability.
  • RPA and the Mre11-Sae2 complex play crucial roles in preventing the formation and propagation of these unstable DNA structures.
Keywords:
Mre11RPASae2gene amplificationinverted duplicationpalindrome

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