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請用此 Handle URI 來引用此文件: http://tdr.lib.ntu.edu.tw/jspui/handle/123456789/6125
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dc.contributor.advisor謝旭亮(Hsu-Liang Hsieh)
dc.contributor.authorHui-Chen Kuoen
dc.contributor.author郭蕙禎zh_TW
dc.date.accessioned2021-05-16T16:21:28Z-
dc.date.available2018-08-06
dc.date.available2021-05-16T16:21:28Z-
dc.date.copyright2013-08-06
dc.date.issued2013
dc.date.submitted2013-07-29
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dc.identifier.urihttp://tdr.lib.ntu.edu.tw/jspui/handle/123456789/6125-
dc.description.abstract在植物的生長與發育過程中,光扮演著重要的調控角色,而不同波長的光有著不同的影響。在紅光遠比遠紅光低的情況之下,植物會處在類似遮蔭的環境下而產生下胚軸與節間徒長的性狀,如此的表現型被稱為避蔭效應 (Shade avoidance syndrome)。近來已經有許多植物荷爾蒙被發現參與在避蔭效應的調控,而在阿拉伯芥中茉莉酸也被證實會參與其中,但是避蔭效應與茉莉酸之間的交互作用與詳細的訊息傳遞機制卻仍然未知。LONG HYPOCOTYL IN FAR-RED 1 (HFR1)已被發現在避蔭效應的訊息調控中扮演著負調控者的角色,而FAR-RED INSENSITIVE 219 (FIN219) 則在茉莉酸訊息調控中具有正調控者的功能。HFR1和FIN219都已被證實參與phyA和避蔭效應的訊息調控之中,並且也分別被證實會與COP1進行交互作用;為瞭解它們在避蔭效應與茉莉酸訊息傳遞中的調控關係,我們觀察了雙突變株fin219hfr1幼苗,發現其對於茉莉酸的添加具有更不敏感的表現型,但是在低紅光/遠紅光比例下則有更顯著的長下胚軸表現型。在基因表現上顯示HFR1會參與在茉莉酸的訊息傳遞之中,並且會正調控FIN219的表現,而FIN219則會參與在避蔭效應的訊息調控中並負調控HFR1的表現。在蛋白質表現上,則可以發現HFR1會正調控FIN219而FIN219會負調控HFR1的表現,這和基因的表現趨勢相同。在共免疫沉澱檢驗中發現FIN219和HFR1不會有直接的交互作用,因此推測可能還有其他調控者參與在此調控機制之中。綜合研究的結果顯示HFR1以及FIN219在阿拉伯芥生長發育中,對於茉莉酸與遮蔭環境下有著重要的調控功能。zh_TW
dc.description.abstractLight is one of the most effective environment factors that regulate plant growth and development. Different light sources have their own effects on seedlings. Shade-avoidance syndrome (SAS) is the phenotype that occurs at low red to far-red ratio, which will reduce the yield of crops. Although it has been noticed that jasmonates are involved in SAS, the molecular regulation between jasmonates and SAS are still unknown. LONG HYPOCOTYL IN FAR-RED 1 (HFR1) is known as a negative regulator of SAS, and FAR-RED INSENSITIVE 219 (FIN219) is reported to be a positive regulator in JA signaling. Both HFR1 and FIN219 participate in phyA signaling and they are required for SAS. Besides, COP1 has been reported to interact with FIN219 and HFR1, respectively. It is interesting to find the relationship between HFR1 and FIN219, and their regulation during SAS and JA signaling. Here, we found that fin219hfr1 double mutant is insensitive to JA and has even longer hypocotyl phenotype than single mutants in shading treatment. Gene expression analyzer indicated that HFR1 also participates in JA signaling and positively regulates FIN219 expression, whereas FIN219 participates in SAS signaling and negatively regulates HFR1 expression. Protein expression studies showed the same regulatory patterns of FIN219 and HFR1. Moreover, co-immunoprecipitation studies indicated that FIN219 and HFR1 did not physically interact with each other, which implies that other regulators may be involved in this regulation mechanism. Taken together, our data indicate that FIN219 and HFR1 play vital roles in regulating seedling development in response to JA and shading conditions.en
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dc.description.tableofcontentsINTRODUCTION 1
Light and Photoreceptors 1
Shade Avoidance Syndrome 2
Shade Avoidance Response and Photoreceptors 3
Shade Avoidance Response and Hormones 4
Jasmonates 6
JA synthesis and signaling pathway 6
Negative Regulator in SAS signaling: HFR1 8
Positive Regulator in JA signaling: FIN219 9
The Crosstalk between SAS and JA Signaling 10
The Objective of Cross-talk Research 10
MATERIAL AND METHODS 12
Plant Materials 12
Plant Growth Conditions 12
Plasmid Construction 14
Protein Co-IP 14
Total Protein Isolation and Western Blotting 14
Total RNA Isolation and RT-PCR 15
Total Genomic DNA Isolation 15
Measurement of Hypocotyls and Roots 16
Observation of Anthers 16
Chlorophyll Extraction and Quantifications 16
Anthocyanin Extraction and Quantifications 17
RESULTS 18
FIN219 and HFR1 synergistically regulate fertility and stamen elongation. 18
FIN219 and HFR1 participated in JA-regulated responses of root elongation, anthocyanin synthesis and chlorophyll reduction. 18
FIN219 and HFR1 are positive regulators of hypocotyls elongation in various light conditions except for red light. 19
FIN219 and HFR1 are positive regulators in both FR light and JA signalings. 20
FIN219 and HFR1 are negative regulators in low R: FR light condition. 21
HFR1 overexpression rescued the phenotypes of hfr1. 22
Both FIN219 and HFR1 may regulate with each other in the dark or FR light. 22
FIN219 and HFR1 affect the expression of JA biosynthesis genes in both the dark and FR light. 23
HFR1 and FIN219 proteins were induced by low R: FR treatment. 24
FIN219 and HFR1 participated in JA and SAS signaling. 25
phyA and cry1 showed strong inhibition of hypocotyl elongation by methyl JA (MeJA). 26
FIN219 and HFR1 were regulated by photoreceptors in response to low R: FR condition. 27
HFR1 might not physically interact with FIN219 in shading condition. 27
DISCUSSION 28
Phenotypic analysis showed that fin219hfr1 was insensitive to MeJA. 28
fin219hfr1 was insensitive to MeJA and showed a longer hypocotyl than wild type under FR light and low R: FR condition. 30
Both gene and protein expression indicated that HFR1 induced the expression of FIN219, whereas FIN219 repressed the expression of HFR1. 32
FIN219 and HFR1 affect the components of JA biosynthesis and signaling. 33
PIL1, ATHB2 and PIF4 were induced in hfr1-201, but reduced in fin219-2 under shading condition. 34
JA serves as a negative role in SAS signaling and JA signaling genes may be blocked in shading condition.. 35
Photoreceptors phyA, phyB, cry1 and cry2 all regulated the expression of FIN219 and HFR1. 36
HFR1 might not physically interact with FIN219 in shading condition. 37
FIGURES 39
REFERENCES 60
APPENDIX I 67
APPENDIX II 69
APPENDIX III 70
APPENDIX IV 71
APPENDIX V 72
dc.language.isoen
dc.title在阿拉伯芥避蔭效應與茉莉酸訊息傳遞中FIN219與HFR1調控關係的功能性研究zh_TW
dc.titleFunctional Studies of FIN219 and HFR1 Regulatory Relationship in the Integration of Shade Avoidance Syndrome and Jasmonate Signaling in Arabidopsisen
dc.typeThesis
dc.date.schoolyear101-2
dc.description.degree碩士
dc.contributor.oralexamcommittee顏宏真(Hung-Chen Yen),吳素幸(Shu-Hsing Wu),鄭萬興(Wan-Hsing Cheng),涂世隆(Shih-Long Tu)
dc.subject.keyword避蔭效應,茉莉酸訊息傳遞,FIN219,HFR1,zh_TW
dc.subject.keywordShade Avoidance,Jasmonate Signaling,FIN219,HFR1,en
dc.relation.page72
dc.rights.note同意授權(全球公開)
dc.date.accepted2013-07-29
dc.contributor.author-college生命科學院zh_TW
dc.contributor.author-dept植物科學研究所zh_TW
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