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Nanopore sequencing reveals that DNA replication compartmentalisation dictates genome stability and instability in Trypanosoma brucei

Author

Listed:
  • Marija Krasiļņikova

    (120 University Place)

  • Catarina A. Marques

    (120 University Place)

  • Emma M. Briggs

    (120 University Place
    School of Biological Sciences
    Framlington Place)

  • Craig Lapsley

    (120 University Place)

  • Graham Hamilton

    (Bearsden)

  • Dario Beraldi

    (120 University Place)

  • Kathryn Crouch

    (120 University Place)

  • Richard McCulloch

    (120 University Place)

Abstract

The Trypanosoma brucei genome is structurally complex. Eleven megabase-sized chromosomes each comprise a transcribed core flanked by silent subtelomeres, housing thousands of Variant Surface Glycoprotein (VSG) genes. Additionally, hundreds of sub-megabase chromosomes contain 177 bp repeats of unknown function, and VSG transcription sites localise to many telomeres. DNA replication dynamics have only been described in the megabase chromosome cores, and in the single active VSG transcription site. Using a Nanopore genome assembly, we show that megabase chromosome subtelomeres display a paucity of replication initiation events relative to the core, correlating with increased instability. In addition, replication of the active VSG transcription site is shown to originate from the telomere, likely causing targeted VSG recombination. Lastly, we provide evidence that the 177 bp repeats act as conserved DNA replication origins, explaining submegabase chromosome stability. Compartmentalized DNA replication therefore explains how T. brucei balances stable genome transmission with localised instability driving immune evasion.

Suggested Citation

  • Marija Krasiļņikova & Catarina A. Marques & Emma M. Briggs & Craig Lapsley & Graham Hamilton & Dario Beraldi & Kathryn Crouch & Richard McCulloch, 2025. "Nanopore sequencing reveals that DNA replication compartmentalisation dictates genome stability and instability in Trypanosoma brucei," Nature Communications, Nature, vol. 16(1), pages 1-17, December.
    • Handle: RePEc:nat:natcom:v:16:y:2025:i:1:d:10.1038_s41467-025-56087-3
    DOI: 10.1038/s41467-025-56087-3
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