Publication | Closed Access
Evidence that Prohexadione-Calcium Induces Structural Resistance to Fire Blight Infection
30
Citations
29
References
2009
Year
BotanyFire Blight InfectionPathologyPlant PathologyPlant Growth RegulatorTree DiseasePlant-pathogen InteractionPhysiological Plant PathologyExperimental ToxicologyCell WallBiologyDisease SeverityNatural SciencesPathogenesisMicrobiologyShoot-growth Regulator Prohexadione-calciumHost ResistanceMedicinePlant Physiology
Mechanisms of fire blight control by the shoot-growth regulator prohexadione-calcium (ProCa) were investigated by comparing disease development in ProCa-treated potted apple trees (cv. Gala) to paclobutrazol (another shoot-growth regulator)-treated and nontreated trees and in ProCa-treated cv. McIntosh trees in the field. Twenty-eight days after inoculation with Erwinia amylovora Ea110, disease incidence on ProCa- and paclobutrazol-treated shoots was significantly reduced compared with that on nontreated shoots. Disease severity (percent shoot length infected) was also significantly lower on both ProCa- and paclobutrazol-treated shoots than on nontreated shoots. However, bacterial populations within inoculated shoots were high and bacterial growth occurred in all treatments. In addition, the mean cell wall width of the cortical parenchyma midvein tissue of the first and second youngest unfolded leaves of ProCa- and paclobutrazol-treated shoots was significantly wider both 0.5 and 2 cm from the leaf tips compared with the cell walls of the nontreated tissue. Taken together, these results suggest that reduction of fire blight symptoms by ProCa and paclobutrazol is not the result of reduced populations of E. amylovora in shoots. Moreover, because paclobutrazol also reduced disease severity and incidence, changes in flavonoid metabolism induced by ProCa but not paclobutrazol does not appear to be responsible for disease control as suggested in recent literature. Finally, although this study did not directly link disease control to the observed cell wall changes, the possibility that an increase in cell wall width impedes the spread of E. amylovora should be investigated in more depth.
| Year | Citations | |
|---|---|---|
Page 1
Page 1