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Basal body multipotency and axonemal remodelling are two pathways to a 9+0 flagellum

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  • R. J. Wheeler

    (Sir William Dunn School of Pathology, University of Oxford
    Present address: Max Planck Institute of Molecular Cell Biology and Genetics, Pfotenhauerstraße 108, 01307 Dresden, Germany)

  • E. Gluenz

    (Sir William Dunn School of Pathology, University of Oxford)

  • K. Gull

    (Sir William Dunn School of Pathology, University of Oxford)

Abstract

Eukaryotic cilia/flagella exhibit two characteristic ultrastructures reflecting two main functions; a 9+2 axoneme for motility and a 9+0 axoneme for sensation and signalling. Whether, and if so how, they interconvert is unclear. Here we analyse flagellum length, structure and molecular composition changes in the unicellular eukaryotic parasite Leishmania during the transformation of a life cycle stage with a 9+2 axoneme (the promastigote) to one with a 9+0 axoneme (the amastigote). We show 9+0 axonemes can be generated by two pathways: by de novo formation and by restructuring of existing 9+2 axonemes associated with decreased intraflagellar transport. Furthermore, pro-basal bodies formed under conditions conducive for 9+2 axoneme formation can form a 9+0 axoneme de novo. We conclude that pro-centrioles/pro-basal bodies are multipotent and not committed to form either a 9+2 or 9+0 axoneme. In an alternative pathway structures can also be removed from existing 9+2 axonemes to convert them to 9+0.

Suggested Citation

  • R. J. Wheeler & E. Gluenz & K. Gull, 2015. "Basal body multipotency and axonemal remodelling are two pathways to a 9+0 flagellum," Nature Communications, Nature, vol. 6(1), pages 1-12, December.
    • Handle: RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms9964
    DOI: 10.1038/ncomms9964
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