Mutations in PKA-RI disrupt PKA activity (picomoles per minute per microgram) in the absence of, but not at saturating concentrations of, exogenous cAMP
| [cAMP] (μm) | Strain | Specific activity ± SEM (pmol·min−1·μg−1 |
|---|---|---|
| Can-S | 13.7 ± 1.1 | |
| 11D4/715 | 17.7 ± 0.8 | |
| 0a | ||
| 11D4 | 16.1 ± 0.8 | |
| 715 | 17.0 ± 0.9 | |
| Can-S | 80.1 ± 5.4 | |
| 11D4/715 | 67.3 ± 6.4 | |
| 51-b | ||
| 11D4 | 74.8 ± 6.8 | |
| 715 | 75.2 ± 4.2 |
F1-a Specific PKA activity was quantified in normal and mutant flies in the absence of any exogenous cAMP ([cAMP = 0]). Planned comparisons between group means after a one-way ANOVA (see Materials and Methods) revealed no significant differences between each homozygous mutant (11D4 or715) and the heteroallelic mutant (715/11D4)(p = 0.13 and p = 0.49, respectively) but a significant difference between the average of these three mutant groups and that of wild-type (Can-S) flies (p < 0.006). n = 4 reactions per group, two from each of two replicate tissue homogenates.
↵F1-b Specific PKA activity was quantified in normal and mutant flies at a saturating concentration of exogenous cAMP ([cAMP = 5]). Planned comparisons between group means after a one-way ANOVA (see Materials and Methods) revealed no significant differences between each homozygous mutant (11D4 or715) and the heteroallelic mutant (715/11D4)(p = 0.43 and p = 0.41, respectively) or between the average of these three mutant groups and that of wild-type (Can-S) flies (p = 0.33).n = 4 reactions per group, two from each of two replicate tissue homogenates.