Table III.

Influence of protein kinase and phosphatase inhibitors on [3H]NAA accumulation

Treatment[3H]NAA Accumulation
InhibitorsConcentrationDurationDiffusive componentEfflux component
μmh% control
Protein kinase
 Staurosporine (6)10.5102  ± 132  ± 4
 K252a (3)0.50.598  ± 238  ± 8
 H7 (3)150.5102  ± 5104  ± 5
 W7 (3)150.5109  ± 2110  ± 14
 DMAP2-a(4)2500.5109  ± 484  ± 9
Protein phosphatase
 Calyculin A (2)0.20.595  ± 143  ± 5
 Cantharidin (7)50176  ± 223  ± 5
 Microcystin-LR (3)11104  ± 3105  ± 4
 Okadaic acid (2)0.75195  ± 189  ± 10

Tobacco cells were incubated for the indicated times with inhibitors or the organic solvent (DMSO or ethanol) used to solubilize inhibitors (control cells). The 30-s accumulation of [3H]NAA (19–37 nm external concentration) was monitored as described in “Materials and Methods,” the diffusive component being measured in the presence of 50 μm unlabeled 1-NAA and uncorrected for contamination by the incubation medium. The carrier-mediated component was calculated by subtracting the radioactivity measured in the absence of unlabeled auxin from the diffusive component. Data are means ± se of values obtained in the number of independent experiments given in parentheses, each with three replicates.

    • F2-a DMAP, 6-Dimethylaminopurine.