Articles
INVESTIGATING MECHANISMS OF FIRE BLIGHT CONTROL BY PROHEXADIONE-CALCIUM
Article number
793_48
Pages
325 – 329
Language
English
Abstract
The incidence and severity of fire blight, caused by Erwinia amylovora (Ea), can be reduced by the shoot-growth regulator prohexadione-calcium (ProCa). However, the level of control can be variable.
To begin to investigate the mechanisms of control, ProCa or paclobutrazol, another shoot-growth regulator, was applied to potted apple trees (cv.
Gala) in two field experiments.
Shoots were later inoculated with Ea strain 110, and shoot growth and disease development was followed over 25 days.
Both ProCa and paclobutrazol significantly (P≤0.05) inhibited shoot growth in comparison to non-treated trees.
At both the initiation and conclusion of the experiment, the CFUs/shoot of Ea did not differ significantly among treatments, and Ea was found throughout most shoots.
However, the reduction of disease incidence on ProCa-treated shoots (19.1%) was significant compared to that on both paclobutrazol- (33.3%) and non-treated shoots (61.1%). Differences in incidence between paclobutrazol and non-treated shoots were not significant.
Disease severity, expressed as length of lesion/length of current season’s growth x 100, was significantly lower on both ProCa- and paclobutrazol-treated shoots (5.2±4.7 and 15.9±7.3, respectively with S.E.) than on non-treated (51.6±11.3) shoots.
These results indicate that disease control by ProCa and paclobutrazol is not the result of inhibited movement or killing of Ea in shoots.
In addition, since paclobutrazol also reduced severity and incidence, changes in flavonoid metabolism induced by ProCa but not paclobutrazol may not be primarily responsible for control of fire blight as suggested in recent literature.
To begin to investigate the mechanisms of control, ProCa or paclobutrazol, another shoot-growth regulator, was applied to potted apple trees (cv.
Gala) in two field experiments.
Shoots were later inoculated with Ea strain 110, and shoot growth and disease development was followed over 25 days.
Both ProCa and paclobutrazol significantly (P≤0.05) inhibited shoot growth in comparison to non-treated trees.
At both the initiation and conclusion of the experiment, the CFUs/shoot of Ea did not differ significantly among treatments, and Ea was found throughout most shoots.
However, the reduction of disease incidence on ProCa-treated shoots (19.1%) was significant compared to that on both paclobutrazol- (33.3%) and non-treated shoots (61.1%). Differences in incidence between paclobutrazol and non-treated shoots were not significant.
Disease severity, expressed as length of lesion/length of current season’s growth x 100, was significantly lower on both ProCa- and paclobutrazol-treated shoots (5.2±4.7 and 15.9±7.3, respectively with S.E.) than on non-treated (51.6±11.3) shoots.
These results indicate that disease control by ProCa and paclobutrazol is not the result of inhibited movement or killing of Ea in shoots.
In addition, since paclobutrazol also reduced severity and incidence, changes in flavonoid metabolism induced by ProCa but not paclobutrazol may not be primarily responsible for control of fire blight as suggested in recent literature.
Publication
Authors
M.J. McGrath, G.W. Sundin, M.M. Kennelly
Keywords
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