Title page for etd-0701116-143142


[Back to Results | New Search]

URN etd-0701116-143142
Author Wan-jhen Li
Author's Email Address No Public.
Statistics This thesis had been viewed 5568 times. Download 0 times.
Department Biological Sciences
Year 2015
Semester 2
Degree Master
Type of Document
Language zh-TW.Big5 Chinese
Title Endogenous NO and H2O2 participate in NaCl-mediated leaf senescence via modulating ethylene signaling, biosynthesis and senescence-associated gene expression in sweet potato
Date of Defense 2016-07-19
Page Count 88
Keyword
  • ethylene transduction gene
  • leaf senescence
  • NaCl stress
  • hydrogen peroxide
  • nitric oxide
  • Abstract Leaf senescence is the final stage of leaf develpment and is affected by abiotic and biotic stresses. NaCl stress, one of the important abiotic stresses, may cause early leaf senescence and severe crop yield reduction. Elevation of endogenous NO and H2O2 levels at early stage can act as signal molecules of second messengers. However, their physiological function and possible mechanisms in NaCl-mediated leaf senescence in sweet potato are unclear. In this report, NaCl stress (140 mM) significantly promoted leaf senescence of sweet potato on days 6 and 9 after treatment demonstrated by morphology senescent leaf, reduced chlorophyll content, decreased Fv/Fm level, and elevated NO/H2O2/MDA amounts. A significant elevation of NO and H2O2 amounts were also found within 24 h in NaCl-treated leaves. For endogenous NO as a signal molecule, pretreatment of inhibitors/effectors such as NO scavenger PTIO, nitric oxide synthase (NOS) inhibitor (L-NAME), and nitrite reductase (NR) inhibitor (tungstate) attenuated the NaCl-enhanced NO accumulation within the first 24 h and delayed leaf senescence on days 6 and 9. The source of endogenous NO may partly be synthesized by the NOS and NR activities. Pretreatment of NO donor SNP repressed the PTIO effects and reversed it to a senescent level similar to NaCl alone. For endogenous H2O2 as a signal molecule, pretreatment of inhibitors/effectors such as reduced glutathione (GSH) and NADPH oxidase inhibitor also attenuated the NaCl-enhanced H2O2 accumulation within the first 24 h and delayed leaf senescence on days 6 and 9. The source of endogenous H2O2 may partly come from the NADPH oxidase. Pretreatment of inhibitors/effectors such as PTIO, SNP, GSH, and DPI also repressed gene expression related to NaCl-induced ethylene signal components, ethylene biosynthesis, glutathione-ascorbate cycle, and leaf senescence. These results suggested that endogenous NO and H2O2 accumulation may function as downstream signal molecules of NaCl stress to induce leaf senescence possibly via the modulation of gene expression related to ethylene signal components, ethylene biosynthesis, glutathione-ascorbate cycle, and leaf senescence.
    Advisory Committee
  • Guan-jhong Huang - chair
  • Rong-Fong Lin - co-chair
  • Hsien-Jung Chen - advisor
  • Files
  • etd-0701116-143142.pdf
  • Indicate in-campus at 5 year and off-campus access at 5 year.
    Date of Submission 2016-08-01

    [Back to Results | New Search]


    Browse | Search All Available ETDs

    If you have more questions or technical problems, please contact eThesys