TABLE 2.
VSG loci and activation events
| Relapse peak | VSG | Activation mechanism | Silent gene
|
Activated gene
|
||
|---|---|---|---|---|---|---|
| No. and locationc | No. of minichromosomal genes | BES chromosome size | 1.2 VSG | |||
| First | 1.25 | Duplication | 2 Telo | 1 | 1.8 Mbd | Lost |
| 1.25a | Duplication | 1 Telo | 1 | |||
| 1.67 | In situ | 1 Telo | 0 | 1.8 Mb | Retained | |
| 1.68 | Unknownb | 1 Telo, 1 int | 1 | 1.8 Mb | Lost | |
| 1.69 | Duplication | 2 Telo | 1 | 1.8 Mb | Lost | |
| 1.21 | Duplication | 1 Telo | 1 | 1.8 Mb | Lost | |
| 1.64 | Duplication | 1 Telo | 0 | 1.8 Mb | Lost | |
| Second | 1.23 | Duplication | 2 Telo | 1 | ND | ND |
| 1.70 | Duplication | 2 Telo | 0 | ND | ND | |
| 1.71 | Duplication | 1 Int | 0 | ND | ND | |
| 1.22 | Duplication | 1 Telo | 0 | ND | ND | |
| 1.72 | Duplication | 1 Telo, 2 int | 1 | ND | ND | |
a
Trypanosomes from the mouse experiment.
b
Activation appeared to involve duplication and another event.
c
Telo, in the telomere; int, apparently chromosome internal.
d
Four chromosomes appear to comigrate at 1.8 Mb. We infer from the pattern of ILTat 1.2 VSG loss that all duplicative activations in the first relapse peak converted the same BES, while the ILTat 1.67 VSG occupies a separate chromosome in which it was activated in situ. ND, not determined.