Abstract
African trypanosomes activate, one at a time, a large set of genes coding for different variant-specific surface antigens (VSAs). These genes have been classed into two groups. In the first group a permanently silent basic gene copy is duplicated and the expression-linked copy (ELC) transposed to an expression site located at a chromosome end. The process is a gene conversion which changes a variable stretch of the preceding ELC. Genes belonging to the second group do not give rise to an additional copy when expressed by a still unknown mechanism. We report here that the gene for antigenic type AnTat 1.6 is located in a telomeric DNA region and is expressed without being duplicated. In clone AnTat 1.6 and the ensuing ones, the ELC of the preceding VSA (AnTat 1.3) is conserved, but in a inactive conformation. Moreover, the AnTat 1.6 gene is lost from the genome of the AnTat 1.6-derived variants, in which the duplication-linked mechanism of gene activation occurs: the gene appears to be replaced by the incoming ELC. These observations show that a trypanosome surface antigen repertoire may evolve by loss and gain of VSA genes, depending on the alternation of the different recombinational mechanism involved in antigenic variation.
| Original language | English |
|---|---|
| Journal | Nature |
| Volume | 308 |
| Issue number | 5957 |
| Pages (from-to) | 370-373 |
| ISSN | 0028-0836 |
| DOIs | |
| Publication status | Published - 1984 |
Keywords
- B780-tropical-medicine
- Protozoal diseases
- Trypanosomiasis-African
- Sleeping sickness
- Trypanosoma brucei
- Vectors
- Tsetse flies
- Glossina
- Genes
- Surface antigen
- Repertoire
- Conversion
- Evolution
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