Title page for etd-0706115-060453


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URN etd-0706115-060453
Author MUFIDAH AFIYANTI
Author's Email Address No Public.
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Department Biological Sciences
Year 2015
Semester 2
Degree Ph.D.
Type of Document
Language English
Title Study the role of nitric oxide in the modulation of ethephon or NaCl-induced leaf senescence in sweet potato
Date of Defense 2015-07-06
Page Count 234
Keyword
  • Leaf senescence
  • Ethylene
  • Sweet potato
  • Glutathione
  • Nitric oxide
  • NaCl stress
  • Abstract ABSTRACT
    Leaf senescence has been recognized as the final stage of leaf development and is affected by developmental cues and environmental stimuli, including plant growth regulators such as ethylene, and abiotic stress such as salt (NaCl) stress. In sweet potato, ethephon, an ethylene releasing compound, and NaCl stress could accelerate leaf senescence as demonstrated by elevation of nitric oxide (NO), H2O2, malondialdehyde (MDA), membrane electrolyte leakage, senescence-associated gene expression, reduction of chlorophyll content, decline of Fv/Fm level and leaf yellowing. NO is a gaseous free radical and plays pivotal roles as a signal molecule and source of reactive nitrogen species (RNS) damage in plant development and stress response. The roles of exogenous NO and endogenous NO in association with ethephon and NaCl-induced leaf senescence were not clear in sweet potato. 
    For exogenous NO, application of sodium nitroprusside (SNP; an NO donor) could provide protection against ethephon-induced leaf senescence. The mechanism of NO protection involves the regulation of catalase and calmodulin. Catalase SPCAT1 is the major isoform and H2O2 scavenger in sweet potato leaves, and its enzymatic activity is modulated by calcium and calmodulin SPCAM. Exogenous NO drastically reduced calmodulin SPCAM and catalase SPCAT1 protein levels and enzymatic activity starting from 1 h in ethephon-treated leaves via mechanisms associated with (1) generation of peroxynitrite (likely from exogenous NO reacting with superoxide) and (2) elevation of GSNOR activity and GSSG amount, which in turn lead to protein S-nitrosylation, ubiquitination and 26S proteasome degradation. The decreased catalase combined with enhanced superoxide dismutase (SOD) activities resulted in H2O2 increase at 1 h in treated leaves, which in turn repressed the ethephon signal for inducible gene expression. Those alterations in signal redox components finally result in protection against ethepon-induced leaf senescence.
    For endogenous NO, it was produced at 2 h in treated leaves and could act as a downstream signal component of ethephon leading to leaf senescence, which was eliminated and mitigated by PTIO (an NO scavenger). Senescence-associated markers as mentioned above were also attenuated and associated with the alteration in glutathione redox balance, modulation of catalase SPCAT1 and calmodulin SPCAM protein levels and enzymatic activity via protein S-nitrosylation and ubiquitination. Senescence in sweet potato leaves was also induced by NaCl stress. Endogenous NO gradually increased and accumulated in NaCl-treated leaves within the first 24 h, and likely acted as a downstream signal component of NaCl stress leading to leaf senescence and changes of senescence-associated markers, which were attenuated in NaCl-treated leaves by PTIO. Modulation of catalase SPCAT1 and calmodulin SPCAM protein S-nitrosylation and ubiquitinations were also involved in NaCl-induced leaf senescence.
    Based on these dada, NO can function as a upstream or downstream signal in the modulation of leaf senescence induced by ethephon or NaCl. Exogenous NO can function as an upstream signal to counteract ethephon action with multiple diverse mechanisms, which leads to the protection against leaf senescence. Endogenous NO can be generated and function as a downstream signal of ethephon and NaCl stress, which execute ethephon and NaCl action leading to promotion of leaf senescence.
    Advisory Committee
  • Tse-Min Lee - chair
  • Rong-Fong Lin - co-chair
  • Kuei-Shu Tung - co-chair
  • Ching-Nen Nathan Chen - co-chair
  • Guan-jhong Huang - co-chair
  • Hsien-Jung Chen - advisor
  • Files
  • etd-0706115-060453.pdf
  • Indicate in-campus at 5 year and off-campus access at 5 year.
    Date of Submission 2015-08-06

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