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完整後設資料紀錄
DC 欄位 | 值 | 語言 |
---|---|---|
dc.contributor.advisor | 金洛仁 | |
dc.contributor.author | Po-Wen Chen | en |
dc.contributor.author | 陳柏文 | zh_TW |
dc.date.accessioned | 2021-06-16T17:58:11Z | - |
dc.date.available | 2012-08-17 | |
dc.date.copyright | 2012-08-17 | |
dc.date.issued | 2012 | |
dc.date.submitted | 2012-08-10 | |
dc.identifier.citation | Acharya, B., and Assmann, S. (2009) Hormone interactions in stomatal function. Plant Mol. Biol. 69, 451-462.
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dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/64614 | - |
dc.description.abstract | Boosted responsiveness of plant cells to stress at the onset of pathogen- or chemically-induced resistance is called priming. The chemical beta-aminobutyric acid (BABA) enhances Arabidopsis thaliana resistance to hemi-biotrophic bacteria through priming of the salicylic acid (SA) defence response. Whether BABA increases Arabidopsis resistance to necrotrophic bacteria such as Pectobacterium carotovorum subsp. carotovorum (Pcc) is not clear. Here we show that treatment with BABA protects Arabidopsis against the soft-rot pathogen Pcc. BABA did not prime the expression of the jasmonate/ethylene responsive PDF1.2, which up-regulation is usually associated with resistance to necrotrophic pathogens. Expression of the SA marker gene PR1 upon Pcc infection was primed by BABA treatment, but SA defective mutants demonstrated a wild-type level of BABA-induced resistance against Pcc. BABA primed the expression of the pattern-triggered immunity (PTI)-responsive gene FRK1, NHL10 and CYP81F2 after inoculation with Pcc or after treatment with purified bacterial microbe-associated molecular patterns such as flg22 or elf26. PTI-mediated callose deposition was also potentiated in BABA-treated Arabidopsis and BABA boosted Arabidopsis stomatal immunity to Pcc. BABA treatment primed the PTI response in the SA defective mutants sid2-1 and pad4-1. In addition, BABA-priming was associated with open chromatin configurations in promoter region of PTI marker genes. Our data indicate that BABA primes the PTI responses upon necrotrophic bacteria infection and suggest a role for the PTI responses in BABA-induced resistance.
To further investigate the mechanism of BABA induced resistance, the function of AtNUDX25 that is up-regulated by BABA was analyzed. A AtNUDX25 T-DNA insertion knockout line demonstrated increased susceptibility to Pcc and was hyper-sensitive to oxidative stress. These data suggest that AtNUDX25 may play a role in resistance to biotic stress and tolerance to abiotic stress. | en |
dc.description.provenance | Made available in DSpace on 2021-06-16T17:58:11Z (GMT). No. of bitstreams: 1 ntu-101-R99b42030-1.pdf: 3354867 bytes, checksum: 29c8a865a23fabd687684be3482ae3d6 (MD5) Previous issue date: 2012 | en |
dc.description.tableofcontents | Contents
碩士論文口試委員審定書 誌謝 摘要 Abstract Abbreviations PartⅠ Introduction ……………………………………………….………………..…….……1 Materials and Methods ………………………………………………..………………5 1 Biological materials……………………………………………………...…………5 2 Bacterial inoculations……………………………………………………...……….5 3 Quantitative RT-PCR……………………………………………..………………..6 4 BABA treatment…………………………………………………..……………….7 5 MAMP treatments………………………………………………..……….………..8 6 Callose staining………………………………………………..…………….……..8 7 Stomatal assay…………………………………………………………….………..9 8 ChIP assay……………………………………………….………………….……...9 Results …………………………………………………………………………………11 1 BABA-induced resistance to Pcc………………………………………….…………….11 2 Roles of JA and ET defence signalling pathways in BABA-induced resistance to Pcc infection………………………………………………………………………11 3 Priming of the SA-dependent defence signalling cascade by BABA upon Pcc SCC1 infection……………………………………………………………...…….13 4 BABA-induced potentiation of PTI-responsive genes expression and callose deposition……………………………………………………………...………….14 5 Reopening of stomata upon Pcc infection is blocked by BABA……………...….15 6 Priming of the PTI response in SA defective mutants upon Pcc infection………..16 7 BABA induces chromatin modifications associated with transcriptional activation ……………………………………………………………………………………18 Discussion …………………………………………………………………….….……20 Conclusions and Future Perspectives ………………………………………….……27 Figures …………………………………………………………..……...……………..29 1 Enhanced resistance of BABA-treated Arabidopsis to Pcc SCC1 infection…...…29 2 BABA-mediated enhanced resistance at 48 hpi with Pcc SCC1……………….....31 3 Role of JA/ET defence signalling cascades in BABA-induced resistance to Pcc ………………………………………………………………………………...…..32 4 Involvement of SA signalling in BABA-induced resistance to Pcc SCC1….........34 5 Defective PR1 up-regulation in SA mutants…………………………………..….36 6 The Pcc hrp- and hrc-deficient mutant strain WPP17 is less virulent than the wild-type Pcc SCC1 strain……………………………………………………..…37 7 Effect of BABA treatments on the Arabidopsis PTI response……………..……...38 8 BABA primes the PTI response upon infection with wild-type Pcc SCC1 bacteria……………………………………………………………………….…...40 9 BABA effect on stomatal movements upon Pcc SCC1 infection…………….…..42 10 BABA primes the PTI response in SA defective mutants…………………….…..43 11 BABA-mediated priming of PTI upon Pcc SCC1 infection in SA defective mutants…………………………………………………………………….……...45 12 Modifications of histone H3 after BABA treatment……………………………...47 13 Callose deposition in non buffer-infiltrated Arabidopsis leaves………………….49 14 Hypothetical model illustrating BABA-induced resistance to Pcc……………….50 Appendixes ……………………………………………………………………………52 References ……………………………………………………………………….……53 PartⅡ Introduction ……………………………………………………………...……………59 Materials and Methods ………………………………………………………………64 1 Biological materials………………………………………………………….……64 2 BABA treatment……………………………………………………….………….64 3 Pectobacterium carotovorum infection………………………………….………..64 4 Trypan blue staining……………………………………………………..……… 65 5 Treatments of plants with PQ……………………………………………..……..66 Results ………………………………………………………………………..………67 1 The knock-out T-DNA insertion mutant atnudx25 is more sensitive to Pcc…..….67 2 atnudx25 is hypersensitive to oxidative stress………………………………...….68 3 atnudx25 demonstrated wild-type levels of bacteria-mediated programmed cell death………………………………………………………………………………68 Discussion …………………………………………………………………………..…70 Conclusions and Future Perspectives ………………………………………….……72 Figures ………………………………………………………………………...………73 1 The knock-out T-DNA insertion mutant atnudx25 is more sensitive to Pcc……...73 2 The mutant atnudx25 is more sensitive to oxidative stress……………………….74 3 Programmed cell death caused by avirulent Pst avrRpt2 bacteria………………..75 Appendixes ……………………………………………………………………………76 References ……………………………………………………………………….……78 | |
dc.language.iso | en | |
dc.title | 阿拉伯芥透過誘發反應調控先天性免疫作用抵抗死體寄生型之軟腐病原細菌 | zh_TW |
dc.title | Priming of the Arabidopsis Pattern-Triggered Immunity Response upon Infection by Necrotrophic Pectobacterium carotovorum Bacteria | en |
dc.type | Thesis | |
dc.date.schoolyear | 100-2 | |
dc.description.degree | 碩士 | |
dc.contributor.oralexamcommittee | 鄭秋萍,林乃君 | |
dc.subject.keyword | β-氨基丁酸,植物先天性防禦反應,胝質蓄積,誘發反應,軟腐病原菌,氣孔防禦, | zh_TW |
dc.subject.keyword | BABA,pattern-triggered immunity,callose deposition,priming,Pectobacterium carotovorum,stomatal immunity, | en |
dc.relation.page | 81 | |
dc.rights.note | 有償授權 | |
dc.date.accepted | 2012-08-10 | |
dc.contributor.author-college | 生命科學院 | zh_TW |
dc.contributor.author-dept | 植物科學研究所 | zh_TW |
顯示於系所單位: | 植物科學研究所 |
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