【作者】 刘勇；

【导师】 王国红； 戈峰；

【作者基本信息】 福建师范大学 ， 动物学， 2011， 硕士

【摘要】 近年来全球大气二氧化碳(C02)浓度呈加速上升的趋势,由此造成的温室效应对人类、环境和生态系统的影响受到国际社会的重视和关注。本论文以模式植物拟南芥(Arabidopsis thaliana)和刺吸式口器昆虫桃蚜(Myzus persicae)为研究对象,以C02浓度升高为作用因子,利用多种拟南芥防御途径缺失的突变体为材料,研究了大气CO2浓度升高对植物诱导抗性以及桃蚜种群适合度的影响。研究表明：(1)大气C02浓度升高增加了野生型(Col-0)和水杨酸途径缺失型(nprl)拟南芥上的桃蚜种群数量,且仅增加了nprl上的桃蚜平均相对生长率；(2)正常C02浓度下,桃蚜为害降低了野生型(Col-0)拟南芥中茉莉酸和乙烯的含量,增加了水杨酸的含量;在桃蚜为害与不为害处理中,C02浓度升高均降低了野生型(Col-0)拟南芥的茉莉酸含量,增加水杨酸含量。(3)高通量转录组测序显示,CO2浓度升高、桃蚜为害及其交互作用均对拟南芥转录组产生影响,诱导大量差异基因的表达,涉及植物150余条代谢通路,根据差异基因的聚类分析,拟南芥转录组表达模式对桃蚜为害的响应变化较CO2因子更为一致。相比之下,CO2浓度升高对桃蚜转录组的影响较小,仅上调了Hspl4,过氧化物酶,细胞色素P450等209个相关基因的表达,下调Hsp60, Hsp70和丝氨酸蛋白酶抑制剂等86个基因的表达。(4)荧光定量PCR结果显示,野生型(Col-0)、茉莉酸途径缺失型(jarl)和乙烯途径缺失型(ein2-5)对桃蚜为害的响应模式较为一致,均在为害后6小时内即可激活以水杨酸(SA)信号途径为主的诱导防御反应,24小时诱导防御反应最为强烈,同时避免或未激活植物茉莉酸(JA)/乙烯(ET)途径相关基因的表达；桃蚜为害没有诱导水杨酸途径缺失型突变体nprl的SA信号途径的诱导防御反应,却上调了JA信号途径的系统防御反应;并且C02浓度升高会增加了三种防御途径缺失型突变体及野生型拟南芥SA防御途径基因的表达,降低JA/ET防御途径基因的表达。本研究清楚地表明：C02浓度升高增强了植物对蚜虫的无效抗性-水杨酸信号途径,削弱了植物对蚜虫的有效抗性-茉莉酸信号途径,从而增加了桃蚜在拟南芥上的种群数量。这是首次从植物诱导抗性角度揭示CO2浓度升高增加桃蚜种群适合度的分子机理,为明确植物-蚜虫对大气CO2浓度升高的响应和适应性机理提供重要的理论基础。更多还原

【Abstract】 As the increases of the concentration of atmospheric carbon dioxide (CO2), the considerable effort has been made to investigate the impact of the greenhouse effects on human, environments and ecosystems around the world. The present study examined the interactions between peach aphid (Myzus persicae) and four Arabidopsis thaliana isogenic genotypes including wild type and three mutants when plants were grown under ambient (370 ppm) and elevated (750 ppm) CO2. We focused on the effect of elevated CO2 on plant induced resistance against aphids. Our data showed that:(1) elevated CO2 increased the population abundance of peach aphid when reared on wild-type (Col-0) and SA-deficient mutants (nprl), and only increased the mean rate growth rate of aphid reared on Col-0 plant. (2)Under ambient CO2, aphid infestation reduced the jasmonic acid and ethylene levels but increased the salicylic acid level in wild-type plant. Regardless of aphid infestation, elevated CO2 decreased the jasmonic acid but increased the salicylic acid level in wild-type plant. (3) By using high-throughput transcriptome sequencing, CO2 level, aphid infestation and their interactions altered the transcription profiles of many genes involved 150 metabolic pathways of plant. According to cluster analysis of differential genes, the consistency of plants transcriptomic expression patterns response to aphid infestation is much better than response to elevated CO2. By contrast, elevated CO2 caused some changes of transcriptome in aphids which up-regulated 209 genes including Hspl4, cytochrome P450 (CYP) and antioxidant enzymes and down-regulated 86 genes including Hsp60, Hsp70 serine proteinase inhibitor. (4) The results from real-time PCR suggested that wild-type, JA-deficient mutants (jarl) and ET-insensetive mutants (ein2-5) had similar response patterns to aphid infestation. Defense genes involved in the salicylic acid (SA) signaling pathways were triggered at 6h and reached maximum expression at 24h since aphid infestation. Meanwhile, the expression of those genes involved in jasmonic acid (JA) and ethylene (ET) signaling pathway were inhibited. However, aphid infestation up-regulated the genes involved in JA defense pathway instead of in SA defense pathway in nprl because of the mutation of SA singaling pathway. Furthermore, for all four genotypes of Arabidopsis, elevated CO2 up-regulated the expression of SA-dependent defense genes but down-regulated the expression of JA-dependent defense genes of plant when infested by aphids. The current study indicated that elevated CO2 tend to enhance the ineffective defense-SA signaling pathway and alleviate the effective defense-JA signaling pathway against aphid, and in turn increased the population abundance of aphids. Our study not only firstly clarified the molecular mechanisms in the increases of the population fitness of aphid response to elevated CO2, but provided the theoretical basis for understanding the adaptation of aphid and its host plant response to elevated CO2.更多还原