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Multiple pathways suppress telomere addition to DNA breaks in the Drosophila germline

Michelle Beaucher1, Xiao-Feng Zheng, Flavia Amariei

  • 1Laboratory of Biochemistry and Molecular Biology, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892, USA.

Genetics
|March 27, 2012
PubMed

Insights

Scientists identified factors that suppress telomere addition at DNA double-strand breaks (DSBs). Disrupting DNA repair or sensing factors increased telomere formation, revealing new insights into chromosome end maintenance.

Area of Science:

  • Molecular Biology
  • Genetics
  • Cell Biology

Background:

  • Telomeres protect chromosome ends from being recognized as DNA double-strand breaks (DSBs).
  • Conversely, de novo telomere addition is suppressed at DSB sites.

Purpose of the Study:

  • To identify factors that suppress de novo telomere formation at DSBs.
  • To investigate the roles of DNA repair and sensing factors in this process.

Main Methods:

  • Developed a novel assay in Drosophila to monitor de novo telomere formation at specific DSB sites induced by I-SceI endonuclease.
  • Quantified telomere formation frequency in various genetic backgrounds with mutations in DNA repair, sensing, or telomere protection factors.

Main Results:

  • Disruption of DNA double-strand break (DSB) repair factors (Rad51, DNA ligase IV) and DSB sensing factors (ATRIP, MDC1) significantly increased de novo telomere formation.
  • Partial disruption of ATM or NBS, factors regulating telomere protection, also enhanced telomere formation, suggesting opposing roles in maintenance versus establishment.
  • In ku70 mutants, telomere establishment was preceded by DSB end degradation.
  • Removal of ATRIP dramatically increased telomeric retrotransposon attachment to broken ends.

Conclusions:

  • Identified key pathways and factors that suppress telomere addition at DSBs.
  • Demonstrated opposing roles for ATM and NBS in telomere maintenance and establishment.
  • Highlighted ATRIP's role in preventing telomeric retrotransposon integration at DSBs.
  • Provided a foundation for future mechanistic studies on telomere regulation at DNA breaks.

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