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Burdock Fructooligosaccharide-induced Priming For Pathogen Resistance Against Pseudomonas Syringae Pv.Tomato DC3000in Arabidopsis Thaliana

Posted on:2015-01-28Degree:DoctorType:Dissertation
Country:ChinaCandidate:Y L GuoFull Text:PDF
GTID:1260330431455276Subject:Biochemistry and Molecular Biology
Abstract/Summary:PDF Full Text Request
Plants can acquire strengthened resistance to pathogens after treatment with incompatible pathogens or elicitors. Elicitors are chemicals or biofactors that can induce plant defense resonses. Burdock fructooligosaccharide (BFO) isolated from the root tissue of Arctium lappa is a reserve carbohydrate. BFO alone has no anti-microbial activities in vitro, but instead, it induces defensive responses in plants as a potential elicitor. BFO can induce resistance against a number of plant diseases, including fungal diseases and virus diseases.This study shows that BFO could increase resistance against Pseudomonas syringae pv. tomato DC3000(Pst DC3000) in Arabidopsis. The growth rate of Pst DC3000declined in Arabidopsis leaves and disease symptoms were suppressed in BFO-pretreated plants. Burdock fructooligosaccharide (BFO) induces plant defense responses through priming, leading to rapid counterattack against pathogen. To investigate the effects of priming by BFO on defense-related responses, Arabidopsis was treated with BFO and the effects of pathogen challenge on cellular and molecular defense responses were analyzed. BFO treatment and subsequent Pseudomonas syringae pv. tomato DC3000challenge triggered earlier expression of defense response genes and pronounced cellular defense events, including a hydrogen peroxide (H2O2) burst, hypersensitive cell death (HCD), and callose deposition. BFO-induced priming was absent in NahG [a transgenic plant that does not accumulate salicylic acid (SA)], sid2(a SA-deficient mutant), and nprl-1(a mutant that carries a deficient NPR1gene), but not in aba3-1[an abscisic acid (ABA)-deficient mutant]. Removal of H2O2by catalase almost completely nullified the cellular and molecular defense responses. Our results indicated that BFO-induced priming is dependent on H2O2, SA and intact NPR1, but is not affected by the ABA signal transduction pathway.To explore whether the disturbed redox homeostasis also functions in BFO-induced priming, we detected the H2O2accumulation, the activities of reactive oxygen species scavengers and the transcription of their encoding genes while reducing reactive oxygen species levels and GST1. The results showed that BFO triggered H2O2accumulation in Arabidopsis during the period tested and the level of H2O2reach the highest at6hours post treatment, but restore to the original level at24hours post treatment. Meanwhile, BFO treatment improved the activities of reactive oxygen species scavengers, the transcription of their encoding genes while reducing reactive oxygen species levels and GST1. These results suggested that the plants have escalated oxidative state. Combined with catalase and Pst DC3000inoculation, we analyzed the cellular defense responses. Catalase, which infiltrated with BFO treatment, nullifies the escalated oxidative state and the augmented ROS accumulation when infected by Pst DC3000. Moreover, the disease resistance was also abolished in BFO pretreated but catalase treated plants, which suggests that the disrupted redox homeostasis is required in BFO-induced priming.Stomatal closure is a part of plant innate immune response to restrict bacterial invasion. In this study, the effects of BFO on stomata movement in Pisum sativum and the possible mechanisms were studied. The results showed that BFO could induce stomatal closure accompanied by ROS and NO production, as is the case with ABA. BFO-induced stomatal closure was inhibited by pre-treatment with L-NAME (NG-nitro-L-arginine methyl ester, hydrochloride; nitric oxide synthase inhibitor) and catalase (hydrogen peroxide scavenger). Exogenous catalase completely restricted BFO-induced production of ROS and NO in guard cells. In contrast, L-NAME prevented the rise in NO levels but only partially restricted the ROS production. These results indicate that BFO-induced stomatal closure is mediated by ROS and ROS-dependent NO production. Another, BFO could also induce stomatal closure in Arabidopsis in this study.
Keywords/Search Tags:Burdock fructooligosaccharide, Priming, H2O2, Stomatal closure
PDF Full Text Request
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