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郭博铖 #, 柯希望 #, 高尚雨, 于昕卉, 孙启明, 左豫虎 *.褪黑素诱导小豆抗锈病机理的初步研究[J].植物保护,2020,46(1):145-150.
褪黑素诱导小豆抗锈病机理的初步研究
A preliminary study on the mechanisms of melatonin induced rust resistance of adzuki bean
投稿时间:2018-12-19  修订日期:2018-12-28
DOI:DOI:10.16688/j.zwbh.2018521
中文关键词:  小豆  小豆锈病  褪黑素  诱导抗性
英文关键词:Vigna angularis  adzuki bean rust  melatonin  induced resistance
基金项目:黑龙江省大学生创新创业训练计划项目(201710223019);国家自然科学基金(31501629);黑龙江省普通本科高等学校青年创新人才培养计划(UNPYSCT-2016201,UNPYSCT-2017113);黑龙江省农垦总局科技计划项目(HNK125B-08-08A);黑龙江八一农垦大学三纵三横团队支持计划(TDJH201801);杂粮特色学科项目
作者单位
郭博铖 #, 柯希望 #, 高尚雨, 于昕卉, 孙启明, 左豫虎 * 黑龙江八一农垦大学农学院, 大庆 163319 
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中文摘要:
      为明确外源褪黑素诱导小豆抗锈性的作用及机理,以感病小豆品种‘宝清红’为材料,采用叶面喷施不同浓度褪黑素激发处理小豆真叶,而后对真叶挑战接种锈菌夏孢子,结果表明,低浓度(11.61 mg/L)褪黑素可显著提升小豆对锈病的抗性。夏孢子萌发试验表明,褪黑素对夏孢子萌发及芽管生长无显著抑制作用,表明褪黑素无抑菌活性。进一步的基因表达分析发现,与对照相比,褪黑素激发诱导了水杨酸(SA)通路关键基因 NPR1 于接种后24 h显著上调表达,且病程相关蛋白PR1、几丁质酶(CHI)、 β-1,3-葡聚糖酶(GLU)及PR5均于接种后24~120 h被显著诱导表达,说明褪黑素可能通过诱导 NPR1 表达,进而激活下游PR蛋白的高水平应答,使感锈病小豆品种获得对锈病的抗性。
英文摘要:
      To understand the role and mechanism of exogenous melatonin in inducing rust ( Uromyces vignae ) resistance of adzuki bean ( Vigna angularis ), the leaves of the susceptible cultivar ‘Baoqinghong’ (BQH) were inoculated with urediniospores after treated with different concentrations of melatonin. The results showed that low concentration (11.61 mg/L) of melatonin could significantly induce rust resistance of the susceptible cultivar BQH.Additionally, urediniospore germination test showed that melatonin had no effect on the urediniospore germination. Subsequently, gene expression analysis of the key gene of salicylic acid (SA) pathway NPR1, compared with mock treatments, showed a significant up regulation at 24 h post inoculation (hpi) pretreated with melatonin. Meanwhile, the expression level of pathogenesis related proteins, including PR1, chitinase (CHI), β-1,3-glucanase (GLU) and PR5 were all induced at 24 to 120 hpi, indicating that melatonin induced adzuki bean resistance against rust infection was closely related to NPR1 induction and the subsequent pathogenesis related protein activation.
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