Table 8.
Btn2 overproduction (from copper promoter) curing in mutants of genes shown to interact with Btn2 (Kama et al. 2007)
| Strain | Btn2 overproduction |
Cur1 overproduction |
||
|---|---|---|---|---|
| Colonies | % Curing | Colonies | % Curing | |
| Wild-type | 637 | 69 | 408 | 59 |
| snc1Δ | 538 | 68 | 349 | 70 |
| snc2Δ | 417 | 87 | 230 | 73 |
| pep8Δ | 301 | 88 | 233 | 81 |
| vps27Δ | 401 | 79 | 559 | 66 |
| tlg2Δ | 224 | 34 | 248 | 50 |
| vps35Δ | 419 | 92 | 433 | 84 |
Strain BY241 (w.t.) and isogenic knockout strains were tested for curing as described in Methods. The stability of [URE3] in the wild-type and mutant strains was tested before introduction of the CUR1/BTN2 overexpression plasmids as well as a 0 mM copper control for the WT (using “copper-free” YNB). Loss of [URE3] was <1% in all of these cases. In all mutants, robust curing was observed by overproduction of either Btn2 or Cur1. While there were statistically significant differences (e.g., the tlg2Δ strain was slightly more slowly for curing by Btn2p, while the pep8 Δ and vps35Δ were slightly more rapidly cured by Btn2 or Cur1, vps27Δ by Cur1 and snc2Δ by Btn2), all were well cured.