Fusicoccin Concentration Research Articles

Responses of Avena Coleoptiles to Suboptimal Fusicoccin: Kinetics and Comparisons with Indoleacetic Acid

Proton excretion induced by optimal concentrations of indoleacetic acid (IAA) and fusicoccin (FC) differs not only in maximum rate of acidification but also in the lag before onset of H(+) excretion and in sensitivity to cycloheximide. Because these differences might simply be a consequence of the difference in rate of proton excretion, FC and IAA have now been compared using oat coleoptiles (cv. Victory) under conditions where the rates of acidification are more similar, i.e. suboptimal FC versus optimal IAA. As the concentration of FC is reduced, the rate of H(+) excretion decreases, the final equilibrium pH increases, and the lag before detectable acidification increases up to 7-fold. This enhanced lag period is not primarily a consequence of wall buffering, inasmuch as it persists when a low concentration of FC is added to sections which were already excreting H(+) in response to IAA. An extended lag also occurs, upon reduction of FC levels, in the hyperpolarization of the membrane potential, before enhancement of O(2) uptake and before the increased rate of Rb(+) uptake. The presence or absence of a lag is not a distinguishing feature between FC and IAA actions on H(+) excretion and cannot be used to discriminate between their sites of action. In contrast, the insensitivity of FC-induced H(+) excretion to cycloheximide, as compared with the nearly complete inhibition of this auxin effect by cycloheximide, persists even at dilute concentrations of FC. This seems to be a basic difference in H(+) excretion by IAA and FC.

Uptake and Transport of Fusicoccin in Higher Plant Tissues

The uptake and release of 3H-labelled fusicoccin (FC) fed to pea internode segments and the transport of [3H]FC in whole plants and in excised parts of plants of pea, maize, and pumpkin have been investigated. FC uptake showed three phases apparently corresponding to the pene tration of FC: (1) into the free space; (2) into the cytoplasm; (3) into the vacuole. The first phase is a little thermosensitive and apparently includes adsorption binding to some free space component (cell surface?). The second and third phases are highly temperature sensitive and in part energy-dependent. However, no accumulation of FC against a concentration gradient is observed at high external FC concentration. Accumulation at low concentration seems due to the formation of a poorly exchangeable complex with some cell structure. The efflux of the FC penetrated within the cells is limited by some highly temperature sensitive process. A small fraction of the accumulated FC tends to be retained in the tissue, either because sequestered in some compartment or because bound to some cellular component. FC transport in whole plants as well as in isolated plant parts seems to depend mainly on simple diffusion and on transport by mass flow in the xylem. Long distance transport of the toxin in pumpkin plants mainly occurs in the xylem, while the slow movement in non-vascular tissues seems to depend on diffusion combined with mass flow in the free space, and does not seem heavily influenced by metabolic factors.

Stomatal response of two almond cultivars to fusicoccin

The leaves of two cultivars of almond ( Prunas amygdalus St.), one (“Filippo Ceo”) resistant and one (“Occhiorosso”) susceptible to the bud canker caused by Fusicoccum amygdali Del., were painted with or allowed to absorb fusicoccin at various concentrations from 2 × 10 −5 m to 2 × 10 −7 m, or control solutions. At various times after treatment, the stomatal resistance to transpiration by the leaves was measured with a ventilated diffusion porometer. Fusicoccin stimulated stomata of both cultivars to open in both the light and dark. The stomata of the resistant cultivar opened more slowly than those of the susceptible cultivar, but little difference in stomatal transpiration between the resistant and susceptible cultivars was observed after either painting with or absorption of fusicoccin. When absorbed into the transpiration stream, low concentrations of fusicoccin accumulated in the leaf to concentrations sufficient to open stomata. Inoculation of almond branches with F. amygdali induced changes in the diffusive resistance of leaves distal to the site of inoculation similar to those induced by absorption of pure fusicoccin preparations. The results show that the resistant cultivar, “Filippo Ceo”, had little capacity to limit the transfer of the toxin to the leaf or to reduce the opening effect of fusicoccin. It is concluded that the major resistance of the cultivar to the disease probably occurs in limiting the development of infection or containment of the toxin at the site of infection.

Effects of Fusicoccin and Kinetin in Isolated Cotyledons of Fenugreek (Trigonella foenum-graecum L.)

Isolated cotyledons of fenugreek (T. foenum-graecum L.) were incubated in darkness and the effects of fusicoccin and kinetin on fresh weight increase and nucleic acid content of the cotyledons, and pH changes of the medium were measured. Both fusicoccin and kinetin stimulated fresh weight increase; KCl doubled the effect of fusicoccin but increased that of kinetin by only 20%; other salts (LiCl, NaCI, NH4Cl) could not replace KCI. The fresh weight increase in the presence of fusicoccin and kinetin together exceeded that in the presence of either alone, over a range of fusicoccin concentrations. Nucleic acid content was increased only marginally by fusicoccin, but substantially by kinetin. In contrast, the pH of the medium was lowered significantly by fusicoccin but not (or marginally) by kinetin. With fusicoccin in the solution, the fresh weight increase was less and later inhibited by cycloheximide than with kinetin in the solution; in the absence of KCI, fusicoccin-induced fresh weight increase was especially insensitive to cycloheximide. The fresh weight increase was not inhibited at all by ethylene or by 2,4-dichlorophenoxyacetic acid with fusicoccin in the solution, but it was significantly inhibited with kinetin in the solution.