Table 1. Effect of midgut-specific gene knockdown on nicotine resistance.
| RNAi system | UAS genotype | Mean nicotine resistance (±1 SD) | ||
|---|---|---|---|---|
| Anterior midgut Gal4 (1099) | Anterior midgut Gal4 (43656) | Posterior midgut Gal4 (1967) | ||
| VDRC-GD | Control (GD) | 0.95 ± 0.032 | 0.96 ± 0.032 | 0.83 ± 0.096 |
| Cyp28d1 | 0.90 ± 0.064* | 0.92 ± 0.039* | 0.88 ± 0.047ns | |
| Cyp28d2 | 0.92 ± 0.050ns | 0.96 ± 0.033ns | 0.89 ± 0.072ns | |
| Ugt86Dd | 0.90 ± 0.070* | 0.90 ± 0.025*** | 0.89 ± 0.093ns | |
| VDRC-KK | Control (KK) | 0.84 ± 0.063 | 0.95 ± 0.032 | 0.73 ± 0.099 |
| Cyp28d1 | 0.77 ± 0.086* | 0.88 ± 0.050** | 0.75 ± 0.085ns | |
| Cyp28d2 | 0.84 ± 0.052ns | 0.93 ± 0.078ns | 0.76 ± 0.124ns | |
| Ugt86Dd | 0.77 ± 0.058* | 0.89 ± 0.053** | 0.75 ± 0.083ns | |
| TRiP | Control (TRiP) | 0.93 ± 0.060 | 0.94 ± 0.050 | 0.70 ± 0.069 |
| Cyp28d1 | 0.83 ± 0.073** | 0.91 ± 0.054ns | 0.78 ± 0.079ns | |
The Gal4-UAS-RNAi system was used to knock down expression of three genes in the midgut. The phenotype of each genotype was tested over 7–10 (mean = 9.5) replicate vials. Each gene knockdown was tested against the relevant co-isogenic control using a t-test (ns P ≥ 0.05, * P < 0.05, ** P < 0.01, *** P < 0.001). The viability of each genotype was tested two to five times in no-drug conditions. These genotype means averaged 0.92, 24/30 of the genotypes have greater no-drug viability than nicotine viability, and for the other six genotypes no-drug viability was at most 4% less than that on nicotine food. These observations suggest the effects of these tissue-specific gene knockdowns are not a result of general defects in viability.