Two mechanisms of expression of a predominant variant antigen gene of Trypanosoma brucei.
African trypanosomes evade the host immune response by periodically switching their variant surface glycoprotein (VSG) coat. The resulting, serologically distinct variant antigenic types (VATs) appear in a loosely ordered sequence and those arising early in infections are termed predominant VATs. VAT switching reflects the successive transcriptional activation of single VSG genes from a large repertoire. Activation of some VSG genes is accomplished by duplication of a previously silent basic copy (BC) gene and insertion of this expression linked copy (ELC) near a chromosomal telomere where is is expressed. However, other VSG genes, always located near a telomere, use a non-duplication activation ( NDA ) mechanism. We report here that the gene encoding the predominant IsTat 1.A VSG can be activated with or without duplication. Four of six independently derived clones activated the 1.A gene without gene duplication or detectable rearrangement. The other two contained an active 1.A ELC, possibly generated by a gene conversion extending to the end of the telomere. The ability to utilize both NDA and ELC mechanisms of gene activation and perhaps an alternative mechanism for gene duplication may account for the fact that VAT 1.A is the most predominant VAT of the IsTaR 1 serodeme .
D002874:Chromosome Mapping; D004262:DNA Restriction Enzymes; D005786:Gene Expression Regulation; D005796:Genes; D006023:Glycoproteins / Q000235:genetics / Q000276:immunology; D015533:Transcriptional Activation; D014346:Trypanosoma brucei brucei / Q000235:genetics* / Q000276:immunology; D014643:Variant Surface Glycoproteins, Trypanosoma
D006023:Glycoproteins; D014643:Variant Surface Glycoproteins, Trypanosoma; D004262:DNA Restriction Enzymes