Response Of Plant Defense Induced By Peach Aphid To Elevated CO₂

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.