Aureobasidium pullulans from the Fire Blight Biocontrol Product, Blossom Protect, Induces Host Resistance in Apple Flowers

被引:12
作者
Zeng, Quan [1 ]
Johnson, Kenneth B. [2 ]
Mukhtar, Salma [1 ]
Nason, Sara [3 ,4 ]
Huntley, Regan [1 ]
Millet, Felicia [1 ,5 ]
Yang, Ching-Hong [6 ]
Hassani, M. Amine [1 ]
Zuverza-Mena, Nubia [4 ]
Sundin, George W. [7 ]
机构
[1] Connecticut Agr Expt Stn, Dept Plant Pathol & Ecol, New Haven, CT 06511 USA
[2] Oregon State Univ, Dept Bot & Plant Pathol, Corvallis, OR 97331 USA
[3] Connecticut Agr Expt Stn, Dept Environm Sci & Forestry, New Haven, CT 06511 USA
[4] Connecticut Agr Expt Stn, Dept Analyt Chem, New Haven, CT 06511 USA
[5] Univ Connecticut, Dept Plant Sci & Landscape Architecture, Storrs, CT 06269 USA
[6] Univ Wisconsin, Dept Biol Sci, Milwaukee, WI 53211 USA
[7] Michigan State Univ, Dept Plant Soil & Microbial Sci, E Lansing, MI 48824 USA
基金
美国食品与农业研究所;
关键词
Aureobasidium pullulans; biological control; fire blight; systemic aquired resistance; PSEUDOMONAS-FLUORESCENS A506; BIOLOGICAL-CONTROL AGENT; ACIBENZOLAR-S-METHYL; ERWINIA-AMYLOVORA; POSTHARVEST DECAY; FRUIT; INFECTION; COLONIZATION; INDUCTION; PEAR;
D O I
10.1094/PHYTO-12-22-0452-R
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
Fire blight, caused by Erwinia amylovora, is a devastating disease of apple. Blossom Protect, a product that contains Aureobasidium pullulans as the active ingredient, is one of the most effective biological controls of fire blight. It has been postulated that the mode of action of A. pullulans is to compete against and antagonize epiphytic growth of E. amylovora on flowers, but recent studies have found that flowers treated with Blossom Protect harbored similar to or only slightly reduced E. amylovora populations compared with nontreated flowers. In this study, we tested the hypothesis that A. pullulans-mediated biocontrol of fire blight is the result of induced host resistance. We found that PR genes in the systemic acquired resistance pathway, but not genes in the induced systemic resistance pathway, were induced in hypanthial tissue of apple flowers after the Blossom Protect treatment. Additionally, the induction of PR gene expression was coupled with an increase of plant-derived salicylic acid in this tissue. After inoculation with E. amylovora, PR gene expression was suppressed in nontreated flowers, but in flowers pretreated with Blossom Protect, the heightened PR expression offset the immune repression caused by E. amylovora, and prevented infection. Temporal and spatial analysis of PR gene induction showed that induction of PR genes occurred 2 days after the Blossom Protect treatment, and required direct flower-yeast contact. Finally, we observed deterioration of the epidermal layer of the hypanthium in some of the Blossom Protect-treated flowers, suggesting that PR gene induction in flowers may be a result of pathogenesis by A. pullulans.
引用
收藏
页码:1192 / 1201
页数:10
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