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Molecular and Cellular Biology, September 1999, p. 5839-5846, Vol. 19, No. 9
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.

Predominance of Duplicative VSG Gene Conversion in Antigenic Variation in African Trypanosomes

Nicholas P. Robinson,1 Nils Burman,1,dagger Sara E. Melville,2 and J. David Barry1,*

Wellcome Centre for Molecular Parasitology, University of Glasgow, Anderson College, Glasgow G11 6NU, Scotland,1 and Department of Pathology, Cambridge University, Cambridge CB2 1QP, England2

Received 17 February 1999/Returned for modification 9 April 1999/Accepted 19 June 1999

A number of mechanisms have been described by which African trypanosomes undergo the genetic switches that differentially activate their variant surface glycoprotein genes (VSGs) and bring about antigenic variation. These mechanisms have been observed mainly in trypanosome lines adapted, by rapid syringe passaging, to laboratory conditions. Such "monomorphic" lines, which routinely yield only the proliferative bloodstream form and do not develop through their life cycle, have VSG switch rates up to 4 or 5 orders of magnitude lower than those of nonadapted lines. We have proposed that nonadapted, or pleomorphic, trypanosomes normally have an active VSG switch mechanism, involving gene duplication, that is depressed, or from which a component is absent, in monomorphic lines. We have characterized 88 trypanosome clones from the first two relapse peaks of a single rabbit infection with pleomorphic trypanosomes and shown that they represent 11 different variable antigen types (VATs). The pattern of appearance in the first relapse peak was generally reproducible in three more rabbit infections. Nine of these VATs had activated VSGs by gene duplication, the tenth possibly also had done so, and only one had activated a VSG by the transcriptional switch mechanism that predominates in monomorphic lines. At least 10 of the donor genes have telomeric silent copies, and many reside on minichromosomes. It appears that trypanosome antigenic variation is dominated by one, relatively highly active, mechanism rather than by the plethora of pathways described before.

* Corresponding author. Mailing address: Wellcome Centre for Molecular Parasitology, University of Glasgow, The Anderson College, 56 Dumbarton Rd., Glasgow G11 5JS, Scotland, United Kingdom. Phone: 44 (0)141 330 4875. Fax: 44 (0)141 330 5422. E-mail: j.d.barry{at}bio.gla.ac.uk.

dagger Present address: Department of Laboratory Medicine, County Hospital, Boden, Sweden.

Molecular and Cellular Biology, September 1999, p. 5839-5846, Vol. 19, No. 9
0270-7306/99/$04.00+0
Copyright © 1999, American Society for Microbiology. All rights reserved.


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