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A yeast-endonuclease-generated DNA break induces antigenic switching in Trypanosoma brucei

Author

Listed:
  • Catharine E. Boothroyd

    (Laboratory of Lymphocyte Biology, and,)

  • Oliver Dreesen

    (Laboratory of Molecular Parasitology, The Rockefeller University, New York, New York 10065, USA
    Present address: Institute of Medical Biology, 8A Biomedical Grove, #06-06 Immunos, 138648, Singapore.)

  • Tatyana Leonova

    (Laboratory of Lymphocyte Biology, and,)

  • K. Ina Ly

    (Laboratory of Lymphocyte Biology, and,)

  • Luisa M. Figueiredo

    (Laboratory of Molecular Parasitology, The Rockefeller University, New York, New York 10065, USA)

  • George A. M. Cross

    (Laboratory of Molecular Parasitology, The Rockefeller University, New York, New York 10065, USA)

  • F. Nina Papavasiliou

    (Laboratory of Lymphocyte Biology, and,)

Abstract

Trypanosome glycoprotein switching Sleeping sickness is caused by the trypanosome parasite. This parasite outwits the human immune system by periodically changing its coat protein in a process known as variant surface glycoprotein (VSG) switching. The favoured model to explain switching invokes a normal host process, called gene conversion, that is used to repair DNA. In this work, Nina Papavasiliou and colleagues establish the first in vitro system that recapitulates VSG switching. The data indicate that a spontaneous double-stranded DNA break upstream of the gene encoding the coat protein initiates the process.

Suggested Citation

  • Catharine E. Boothroyd & Oliver Dreesen & Tatyana Leonova & K. Ina Ly & Luisa M. Figueiredo & George A. M. Cross & F. Nina Papavasiliou, 2009. "A yeast-endonuclease-generated DNA break induces antigenic switching in Trypanosoma brucei," Nature, Nature, vol. 459(7244), pages 278-281, May.
    • Handle: RePEc:nat:nature:v:459:y:2009:i:7244:d:10.1038_nature07982
    DOI: 10.1038/nature07982
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    Cited by:

    1. Aditi Mukherjee & Zakir Hossain & Esteban Erben & Shuai Ma & Jun Yong Choi & Hee-Sook Kim, 2023. "Identification of a small-molecule inhibitor that selectively blocks DNA-binding by Trypanosoma brucei replication protein A1," Nature Communications, Nature, vol. 14(1), pages 1-19, December.

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