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| DC 欄位 | 值 | 語言 |
|---|---|---|
| dc.contributor.advisor | 金洛仁(Laurent Zimmerli) | |
| dc.contributor.author | Yu-Hung Yeh | en |
| dc.contributor.author | 葉鈺鴻 | zh_TW |
| dc.date.accessioned | 2021-06-16T22:57:27Z | - |
| dc.date.available | 2017-08-15 | |
| dc.date.copyright | 2012-08-15 | |
| dc.date.issued | 2012 | |
| dc.date.submitted | 2012-08-09 | |
| dc.identifier.citation | References I
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Plant Physiol. 146: 818-824. Herskowitz, I. (1995). MAP kinase pathways in yeast: for mating and more. Cell 80: 187-197. Jakab, G., Cottier, V., Toquin, V., Rigoli, G., Zimmerli, L., Metraux, J.P., and Mauch-Mani, B. (2001). beta-Aminobutyric acid-induced resistance in plants. Eur. J. Plant Pathol. 107: 29-37. Kunze, G., Zipfel, C., Robatzek, S., Niehaus, K., Boller, T., and Felix, G. (2004). The N terminus of bacterial elongation factor Tu elicits innate immunity in Arabidopsis plants. Plant Cell 16: 3496-3507. Melotto, M., Underwood, W., Koczan, J., Nomura, K., and He, S.Y. (2006). Plant stomata function in innate immunity against bacterial invasion. Cell 126: 969-980. Nakagami, H., Pitzschke, A., and Hirt, H. (2005). Emerging MAP kinase pathways in plant stress signalling. Trends Plant Sci. 10: 339-346. Nishimura, M.T., Stein, M., Hou, B.H., Vogel, J.P., Edwards, H., and Somerville, S.C. (2003). Loss of a callose synthase results in salicylic acid-dependent disease resistance. Science 301: 969-972. Roux, M., Schwessinger, B., Albrecht, C., Chinchilla, D., Jones, A., Holton, N., Malinovsky, F.G., Tor, M., de Vries, S., and Zipfel, C. (2011). The arabidopsis leucine-rich repeat receptor-like kinases BAK1/SERK3 and BKK1/SERK4 are required for innate immunity to hemibiotrophic and biotrophic pathogens. Plant Cell 23: 2440-2455. Ton, J., and Mauch-Mani, B. (2004). Beta-amino-butyric acid-induced resistance against necrotrophic pathogens is based on ABA-dependent priming for callose. Plant J. 38: 119-130. Tsai, C.H., Singh, P., Chen, C.W., Thomas, J., Weber, J., Mauch-Mani, B., and Zimmerli, L. (2011). Priming for enhanced defence responses by specific inhibition of the Arabidopsis response to coronatine. Plant J. 65: 469-479. Yuan, J., and He, S.Y. (1996). The Pseudomonas syringae Hrp regulation and secretion system controls the production and secretion of multiple extracellular proteins. J. Bacteriol. 178: 6399-6402. Zimmerli, L., Metraux, J.P., and Mauch-Mani, B. (2001). beta-aminobutyric acid-induced protection of Arabidopsis against the necrotrophic fungus Botrytis cinerea. Plant Physiol. 126: 517-523. Zimmerli, L., Hou, B.H., Tsai, C.H., Jakab, G., Mauch-Mani, B., and Somerville, S. (2008). The xenobiotic beta-aminobutyric acid enhances Arabidopsis thermotolerance. Plant J. 53: 144-156. References II Acharya, B.R., Raina, S., Maqbool, S.B., Jagadeeswaran, G., Mosher, S.L., Appel, H.M., Schultz, J.C., Klessig, D.F., and Raina, R. (2007). Overexpression of CRK13, an Arabidopsis cysteine-rich receptor-like kinase, results in enhanced resistance to Pseudomonas syringae. Plant J. 50: 488-499. Chen, K., Du, L., and Chen, Z. (2003). Sensitization of defense responses and activation of programmed cell death by a pathogen-induced receptor-like protein kinase in Arabidopsis. Plant Mol. Biol. 53: 61-74. Chen, K., Fan, B., Du, L., and Chen, Z. (2004). Activation of hypersensitive cell death by pathogen-induced receptor-like protein kinases from Arabidopsis. Plant Mol. Biol. 56: 271-283. Chen, Z. (2001). A superfamily of proteins with novel cysteine-rich repeats. Plant Physiol. 126: 473-476. Chinchilla, D., Zipfel, C., Robatzek, S., Kemmerling, B., Nurnberger, T., Jones, J.D., Felix, G., and Boller, T. (2007). A flagellin-induced complex of the receptor FLS2 and BAK1 initiates plant defence. Nature 448: 497-500. Czernic, P., Visser, B., Sun, W.N., Savoure, A., Deslandes, L., Marco, Y., Van Montagu, M., and Verbruggen, N. (1999). Characterization of an Arabidopsis thaliana receptor-like protein kinase gene activated by oxidative stress and pathogen attack. Plant J. 18: 321-327. Du, L.Q., and Chen, Z.X. (2000). Identification of genes encoding receptor-like protein kinases as possible targets of pathogen- and salicylic acid-induced WRKY DNA-binding proteins in Arabidopsis. Plant J. 24: 837-847. Nam, K.H., and Li, J. (2002). BRI1/BAK1, a receptor kinase pair mediating brassinosteroid signaling. Cell 110: 203-212. Ohtake, Y., Takahashi, T., and Komeda, Y. (2000). Salicylic acid induces the expression of a number of receptor-like kinase genes in Arabidopsis thaliana. Plant Cell Physiol. 41: 1038-1044. Shiu, S.H., and Bleecker, A.B. (2001). Receptor-like kinases from Arabidopsis form a monophyletic gene family related to animal receptor kinases. Proc. Natl. Acad. Sci. USA 98: 10763-10768. Singh, P., Kuo, Y.C., Mishra, S., Tsai, C.H., Chien, C.C., Chen, C.W., Desclos-Theveniau, M., Chu, P.W., Schulze, B., Chinchilla, D., Boller, T., and Zimmerli, L. (2012). The lectin receptor kinase-VI.2 is required for priming and positively regulates Arabidopsis pattern-triggered immunity. Plant Cell 24: 1256-1270. Tanaka, H., Osakabe, Y., Katsura, S., Mizuno, S., Maruyama, K., Kusakabe, K., Mizoi, J., Shinozaki, K., and Yamaguchi-Shinozaki, K. (2012). Abiotic stress-inducible receptor-like kinases negatively control ABA signaling in Arabidopsis. Plant J. 70: 599-613. Wrzaczek, M., Brosche, M., Salojarvi, J., Kangasjarvi, S., Idanheimo, N., Mersmann, S., Robatzek, S., Karpinski, S., Karpinska, B., and Kangasjarvi, J. (2010). Transcriptional regulation of the CRK/DUF26 group of receptor-like protein kinases by ozone and plant hormones in Arabidopsis. BMC Plant Biol. 10: 95. Zimmermann, P., Laule, O., Schmitz, J., Hruz, T., Bleuler, S., and Gruissem, W. (2008). Genevestigator transcriptome meta-analysis and biomarker search using rice and barley gene expression databases | |
| dc.identifier.uri | http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/64688 | - |
| dc.description.abstract | 摘要一
植物可藉由處理β- aminobutyric acid (BABA) 而增強對病原的抗性，我們在先的研究指出，leucine-rich repeat protein kinase (LRRPK) 可提供植物對抗細菌性斑點病原菌 (Pseudomonas syringae pv. tomato DC3000) 的耐受性，同時，lrrpk對細菌性斑點病原菌的突變株hrcC-也呈現較易感染的情況，因此，LRRPK在植物的免疫反應上是被需要的，lrrpk喪失了BABA在植物被細菌性斑點病原菌感染後對氣孔的調節，lrrpk在處理flg22後也被證實免疫反應的相關基因表現量降低和醣類堆積下降。然而卻沒有改變對Reactive oxygen species 的調控，本研究之目標是尋找LRRPK是否能對抗另外一種病原和分析大量表現LRRPK後植物的表徵，我發現了lrrpk對Pseudomonas syringae pv. maculicola ES4326 (Psm ES4326) 也表現出較易感染的現象，此外，大量表現後的植株對Pst DC3000較有抗性，且在處理flg22後也較多的醣類累積，細菌也無法在3小時後將氣孔重新開啟，結合突變株和大量表現後的植株的實驗，可推論LRRPK參與植物的免疫反應和BABA誘發的防禦反應。 摘要二 DNA微陣列分析，發現了12個多重複半胱胺酸受體激酶，相較於野生株，這12個基因在大量表現凝集素受體激6.2後，至少被誘導了四倍以上，在阿拉伯芥中，多重複半胱胺酸受體激酶(CRK)被歸類成一類的蛋白質受體激酶，在細胞外的區域包含了兩個重複序列C-X8-C-X2-C的模組，目前已經知道，這類的蛋白質受體激酶可以被參與防禦反應的賀爾蒙水楊酸和細菌性斑點病病原菌所誘導表現，在大量表現阿拉伯芥凝集素受體激酶6.2 (LecRK-VI.2) 的在感染細菌性斑點病病原菌 (Pseudomonas syringae pv. tomato DC3000) 後，在插入突變株的分析中，我們並沒有看到任何病徵的改變，這暗示著這些基因在功能上，可能扮演著類似的角色，因此，我們決定分析這12個基因在大量表現後的改變，我們目前的結果顯示，大量表現CRK-H 和CRK-K使植物對細菌性斑點病病原菌有較大之抗性提升，且持續性醣類堆積和免疫相關的基因FRK1與PR1的表現，並使氣孔關閉，由此可以推論CRKs可能與植物的防禦反應有關。 | zh_TW |
| dc.description.abstract | Abstract I
Plants can acquire enhanced resistance to pathogens after treatment with beta- aminobutyric acid (BABA). BABA primes plant’s defense responses. Previously, we showed that a leucine-rich repeat protein kinase (LRRPK) contributes to disease resistance to Pseudomonas syringae pv. tomato (Pst) DC3000. Indeed, lrrpk mutants were more susceptible to Pst DC3000 hrcC-, suggesting this LRRPK is required for pathogen-associated molecular pattern (PAMP)-triggered immunity (PTI). We have demonstrated that lrrpk mutants were defective in BABA-mediated blockage of stomatal reopening after Pst DC3000 infection. lrrpk mutants also demonstrated reduced PTI marker gene induction and impaired callose deposition after flg22 treatment. However, lrrpk mutants demonstrated a normal reactive oxygen species burst. The aim of this study was to identify whether LRRPK can enhance disease resistance to another bacterial pathogen and to analyze the phenotype of LRRPK over-expression (OE) lines. lrrpk mutants were found to be more susceptible to virulent Pseudomonas syringae pv. maculicola (Psm) ES4326 and defective in BABA-mediated plant defense. Moreover, OE lines were more resistant to Pst DC3000 and accumulated more callose after treatment with the PAMP flg22. In addition, stomata of OE lines did not reopen 3 hours post inoculation with bacteria. Knock-out mutants and OE lines phenotypes suggest that LRRPK plays a role in PTI and BABA-induced resistance. Abstract II Genome-wide microarray analysis of an Arabidopsis Lectin Receptor Kinase-VI.2 (LecRK-VI.2) over-expression line shows that 12 cysteine-rich repeat like kinases (Cysteine-rich receptor like kinases, CRK-A, -B, -C, -D. –E, -F, -G, -H, -I , -J, -K, and -L) were up-regulated at least 4-fold when compared to WT. In Arabidopsis, CRKs are a sub-family of receptor-like protein kinases that contain two copies of the C-X8-C-X2-C motif in their extracellular domains. It has been shown that CRK genes can be induced by the defense hormone salicylic acid and bacteria Pst DC3000 (Pseudomonas syringae pv. tomato DC3000) bacteria. Using a T-DNA knock-out approach, we did not observe any altered phenotype after Pst DC3000 inoculation, suggesting that these genes are functionally redundant. Therefore, we decided to use a gain-of-function approach by over-expressing these CRKs in wild-type Col-0 background. Our preliminary results indicate that CRK-H and CRK-K over-expression lines are more resistant to Pst DC3000. In addition, these two CRKs over-expression lines showed constitutive callose deposition and expression of PTI marker gene PR1 (PATHOGENESIS-RELATIVE 1) and FRK1 (FLG22-INDUCED RECEPTOR-LIKE 1), and an altered stomatal immunity. We suggest that CRK-H and CRK-K are involved in plant defense. | en |
| dc.description.provenance | Made available in DSpace on 2021-06-16T22:57:27Z (GMT). No. of bitstreams: 1 ntu-101-R99b42027-1.pdf: 3557357 bytes, checksum: d8f74d389f96d3771ce61cd94f64b59a (MD5) Previous issue date: 2012 | en |
| dc.description.tableofcontents | 摘要一 i
Abstract I ii Abbreviation I iii Introduction I 1 PAMP-Triggered Immunity against Bacterial Pathogens 1 Priming for Enhanced Plant Defense by BABA 2 The characteristics of LRRPK in plant defense 2 Materials and Methods I 4 Biological Materials and Growth Conditions 4 Insertion Mutant Isolation 4 Construction of Transgenic Plants 4 Pst DC3000 and Psm ES4326 Bioassay 5 Botrytis cinerea Bioassay 5 Stomatal Assay 5 Callose Staining 6 Measurement of ROS Production 6 RNA extraction and gene expression analysis 7 Results I 9 Two LRRPK T-DNA Insertion Mutant Lines Are Defective in BABA-Mediated Resistance to Psm ES4326 Bacteria 9 Overexpression of LRRPK Increases Resistance to Pst DC3000 9 Reactive Oxygen Species Production is Not Altered by LRRPK 10 Overexpression of LRRPK Positively Regulates Stomatal Closure after Pst DC3000 Infection 11 Overexpression of LRRPK Increases flg22-Mediated Callose Deposition 11 Overexpression of LRRPK Enhance Disease Resistance to B. cinerea 12 Discussion I 13 LRRPK Positively Regulates the Arabidopsis PTI Response 13 LRRPK Plays a Critical Role in BABA-IR 14 Conclusions and future perspectives I 16 Figures I 17 Figure 1: Putative LRRPK Organization and Analysis of lrrpk1 and lrrpk2 Mutants. 17 Figure 2: BABA-IR in Col-0, lrrpk1 and lrrpk2 Infected with Psm ES4326. 18 Figure 4: LRRPK OE Lines are More Resistant to Pst DC3000. 21 Figure 5: Role of LRRPK in The PTI-Mediated ROS Burst. 22 Figure 6: Over-Expression of LRRPK Alters Stomatal Immunity to Pst DC3000. 23 Figure 7: Ectopic Expression of LRRPK Affects flg22-Mediated Callose Deposition. 24 Figure 8: The Resistance Response of Lines Over-Expressing LRRPK to B. cinerea Infection. 25 Appendixes I 26 Appendix 1: Model for PTI and its Downstream Signaling 26 Appendix 2: BABA-IR in Col-0, lrrpk1 and lrrpk2 Infected with Pst DC3000. 27 Appendix 3: Col-0, lrrpk1 and lrrpk2 Infected with Pst DC3000. 28 Appendix 4: Col-0 and lrrpk Infected with Pst DC3000. 29 Appendix 5: BABA Primes the Arabidopsis PTI Response. 30 Appendix 6: BABA Primes the Arabidopsis PTI Response. 31 Appendix 7: BABA Primes the Arabidopsis stomata closure. 32 References I 33 摘要二 35 Abstract II 36 Abbreviation II 37 Introduction II 38 Materials and Methods II 40 Biological Materials and Growth Conditions 40 Insertion Mutant Isolation 40 Construction of Transgenic Plants 40 Pst DC3000 Bioassay 41 Stomatal Assay 41 Callose Staining 42 RNA extraction and gene expression analysis 42 Results II 44 CRK T-DNA Insertion Mutant Lines Demonstrated Normal Disease Resistance to Pst DC3000 Bacteria 44 Overexpression of CRKs Increases Resistance to Pst DC3000 44 CRK-H or CRK-K Positively Regulates Stomatal Closure upon Pst DC3000 Infection 45 Overexpression of CRK-H or CRK-K Increases Pst DC3000 hrcC- and flg22-Mediated Callose Deposition and Induces a Constitutive Up-Regulation of PTI-Responsive Genes 46 Conclusions and future perspectives II 48 Discussion II 50 Figures II 52 Figure 1: Pst DC3000 infection in Col-0 and 12 crk T-DNA insertion mutant lines. 52 Figure 2: The Full-Length CRKs cDNA are Introduced into pG103 Binary Vector 53 Figure 3: Constitutive Expression of CRK-H in Transgenic Arabidopsis Plants 54 Figure 4: Constitutive Expression of CRK-K in Transgenic Arabidopsis Plants 55 Figure 5: CRK-H OE Lines are more Resistant to Pst DC3000. 57 Figure 6: CRK-K OE Lines are more Resistant to Pst DC3000. 59 Figure 7: Over-Expression of CRK-H Alters Stomatal Immunity to Pst DC3000. 60 Figure 8: Over-Expression of CRK-K Alters Stomatal Immunity to Pst DC3000. 61 Figure 10: Ectopic Expression of CRK-K Affects Pst DC3000 hrcC—and flg22-Mediated Callose Deposition. 65 Figure 11: Ectopic Expression of CRK-H Induces Constitutive expression of PTI marker gene PR1 and FRK1. 66 Figure 12: Ectopic Expression of CRK-K Induced Constitutive expression of PTI marker gene PR1 and FRK1. 67 Appendixe II 68 Appendix 1: Lest of Primers Used for Screening Homozygous crks. 68 Appendix 2: Lest of Primers Used for Transgenics Generation. 69 Appendix 3: Lest of Primers Used for qPCR and RT-PCR 70 Appendix 4: Model for PTI and its Downstream Signalling 71 References II 72 | |
| dc.language.iso | en | |
| dc.subject | 免疫反應 | zh_TW |
| dc.subject | Psm ES4326 | zh_TW |
| dc.subject | 二: | zh_TW |
| dc.subject | DNA微陣列分析 | zh_TW |
| dc.subject | 凝集素受體激酶 | zh_TW |
| dc.subject | 6.2 | zh_TW |
| dc.subject | 細菌性斑點病原菌 | zh_TW |
| dc.subject | 阿拉伯芥 | zh_TW |
| dc.subject | 細菌性斑點病病原菌 | zh_TW |
| dc.subject | leucine-rich repeat protein kinas | zh_TW |
| dc.subject | β- aminobutyric acid | zh_TW |
| dc.subject | 一: | zh_TW |
| dc.subject | 多重複半胱胺酸受體激酶 | zh_TW |
| dc.subject | Genome-wide microarray analysis | en |
| dc.subject | β-aminobutyric acid | en |
| dc.subject | leucine-rich repeat protein kinas | en |
| dc.subject | Pst DC3000 | en |
| dc.subject | pattern-triggered immunity | en |
| dc.subject | Psm ES4326 | en |
| dc.subject | Part II: | en |
| dc.subject | Part I: | en |
| dc.subject | LecRK-VI.2 | en |
| dc.subject | Cysteine-rich receptor like kinases | en |
| dc.subject | Arabidopsis | en |
| dc.subject | Pst DC3000 | en |
| dc.title | 白胺酸重複受體激酶與半胱胺酸重複受體激酶在阿拉伯芥抗病反應之功能性分析 | zh_TW |
| dc.title | Functional Characterization of a Leucine-Rich Repeat and Cysteine-Rich Receptor-Like Kinases Involved in Arabidopsis Defense Responses | en |
| dc.type | Thesis | |
| dc.date.schoolyear | 100-2 | |
| dc.description.degree | 碩士 | |
| dc.contributor.oralexamcommittee | 鄭秋萍(Chiu-Ping Cheng),鄭貽生(Yi-Sheng Cheng) | |
| dc.subject.keyword | 一:,β- aminobutyric acid,leucine-rich repeat protein kinas,細菌性斑點病原菌,免疫反應,Psm ES4326,二:,DNA微陣列分析,凝集素受體激酶,6.2,多重複半胱胺酸受體激酶,阿拉伯芥,細菌性斑點病病原菌, | zh_TW |
| dc.subject.keyword | Part I:,β-aminobutyric acid,leucine-rich repeat protein kinas,Pst DC3000,pattern-triggered immunity,Psm ES4326,Part II:,Genome-wide microarray analysis,LecRK-VI.2,Cysteine-rich receptor like kinases,Arabidopsis,Pst DC3000, | en |
| dc.relation.page | 73 | |
| dc.rights.note | 有償授權 | |
| dc.date.accepted | 2012-08-09 | |
| 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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