Page 114 - 《广西植物》2026年第4期
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treatments: 60%± 2% (water deficit group) and 90% ± 2% (high humidity group). Colony countingꎬ fluorescence
observationꎬ and scanning electron microscopy were employed to investigate the effects and mechanisms of moderate
water deficit treatment on bacterial canker. The results were as follows: (1) Plants under early water deficit treatment
exhibited higher initial enzyme activities of catalase (CAT)ꎬ superoxide dismutase (SOD)ꎬ glutathione reductase (GR)
and phenylalanine ammonia ̄lyase (PAL)ꎬ lower stomatal apertureꎬ and had only about 1/ 5 of the pathogen load in
leaves compared to the high humidity group after 12 days inoculation. (2) When infected plants from the high humidity
group were transferred to water deficit conditionsꎬ leaf fluorescence showed diffuse patterns after 7 daysꎬ and pathogen
mortality reached 99.38% after 12 days of treatmentꎻ this treatment effectively induced a decrease in leaf water potentialꎬ
stomatal closureꎬ and significantly enhanced antioxidant enzyme activities. In conclusionꎬ water deficit reduces pathogen
invasion by decreasing leaf water potential and promoting stomatal closureꎬ while enhancing plant resistance through
antioxidant enzyme regulationꎬ not only inhibiting Psa infection and proliferationꎬ but also eliminating established
pathogens. This study confirms that moderate water deficit effectively controls kiwifruit bacterial cankerꎬ enriches the
“water ̄plant ̄pathogen” interaction framework. It provides new ideas and theoretical references for the prevention and
control of bacterial canker in kiwifruitꎬ and also lays a theoretical foundation for the popularization of field water
management strategies such as rain ̄sheltered cultivation.
Key words: water deficitꎬ bacterial canker of kiwifruitꎬ humidityꎬ resistance mechanismꎬ Pseudomonas syringae
pv. actinidiaeꎬ antioxidant enzymes
猕猴桃原产于中国ꎬ目前中国种植面积和产量 ROS)产生、激活防御相关基因表达等方式增强植物
均居于世界首位(Liu et al.ꎬ 2017)ꎮ 由丁香假单胞 对病原菌的抗性ꎮ Gupta 等(2016) 研究表明ꎬ适度
菌 猕 猴 桃 致 病 变 种 ( Pseudomonas syringae pv. 土壤水分亏缺可降低拟南芥 ROS 产生和细胞死亡ꎬ
actinidiaeꎬPsa)引起的猕猴桃溃疡病严重危害着猕 诱 导 AtPR5、 AtLEA4 等 抗 性 基 因 上 调ꎬ 提 高 对
猴桃产业的发展(Cellini et al.ꎬ 2021)ꎮ 该病具有高 Pseudomonas syringae pv. tomato DC3000 的抗性ꎮ 干
隐蔽性、 高暴发性、 高传染性和高毁灭性等特点 旱适 应 还 可 诱 导 本 生 烟 中 ROS 产 生ꎬ 提 高 对
(Donati et al.ꎬ 2018)ꎬ一旦发生难以治愈ꎮ 该病自 Sclerotinia sclerotiorum 和 Pseudomonas syringae
1989 年在日本被首次报道(Serizawa et al.ꎬ 1989)以 pv. tabaci 的耐受性( Ramegowda et al.ꎬ 2013)ꎮ 但
来ꎬ已在全球主要猕猴桃产区蔓延ꎬ造成严重的产 是ꎬ严重干旱可通过抑制关键免疫因子的表达来削
量和经济损失(Ferrante & Scortichiniꎬ 2009ꎻ Kim et 弱植物防御(Choudhary & Senthil ̄Kumarꎬ 2024)ꎮ
al.ꎬ 2016ꎻ McCann et al.ꎬ 2017)ꎮ 我国于 1985 年在 现有研究表明ꎬ温度是影响溃疡病发生的关键
湖南省东山峰农场首次发现该病ꎬ随后又在多个省 因子ꎬ而雨水主要作为病原菌的传播载体ꎮ 但在实
份暴发ꎮ 2018 年ꎬ该病在福建省福安市暴发ꎬ导致 际生产中发现ꎬ在干旱胁迫下感病叶片会产生大块
2 的与通常的多角形叶溃疡症状不一样的坏死性病
果园株发病率在 70%以上ꎬ超过 15 hm 果园被毁ꎬ
造成了严重的经济损失(Dai et al.ꎬ 2019)ꎮ 随着猕 斑(Mauri et al.ꎬ 2016)ꎮ Froud 等(2015) 在探究热
猴桃产业面积的扩大ꎬ溃疡病防控形势日益严峻ꎮ 处理杀死猕猴桃花粉中所携带的溃疡病菌时发现ꎬ
植物常同时面临生物胁迫和非生物胁迫的双 在相同温度和持续时间条件下ꎬ相对湿度越低ꎬ致
重作用ꎮ 非生物胁迫通过影响植物代谢、细胞活 死效率越高ꎮ 可见水分可能不仅起到传播载体的
性、信号转导以及转录调控等途径调控植物-病原 作用ꎬ还可通过增加组织含水量ꎬ作为直接影响因
体 互 作 ( Suzuki et al.ꎬ 2014ꎻ Pandey & Senthil ̄ 子作用于猕猴桃对溃疡病菌的耐受性和发病过程ꎬ
Kumarꎬ 2017ꎻ Zarattini et al.ꎬ 2021)ꎮ 在诸多组合 因此通过水分调控适度降低植株组织含水量ꎬ或许
中ꎬ干旱胁迫对植物病原体互作的影响研究较为深 能预防和抑制溃疡病的发生ꎮ 目前ꎬ我国部分猕猴
入ꎬ其效应取决于胁迫严重程度、发生时间以及植 桃主产区已逐步推广控雨栽培实践ꎬ通过人为调控
物发育阶段ꎬ可能产生不利或有利影响ꎮ 适度干旱 田间水分条件ꎬ减少溃疡病等病害的发生ꎬ但相关
胁迫可 通 过 调 控 活 性 氧 ( reactive oxygen speciesꎬ 调控措施缺乏明确的理论支撑ꎬ亟需从基础研究层

