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پدید آورنده
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رده
کتابخانه
محل استقرار
9780549234494
dltt
Genetic and molecular analyses of Arabidopsis signaling mechanisms in response to environmental stresses
[Book]
2007.
Adviser: Ming-Che Shih.
Source: Dissertation Abstracts International, Volume: 68-09, Section: B, page: 5781.
Thesis (Ph.D.)--The University of Iowa, 2007.
A balance among metabolites of flavonoid biosynthesis is tightly maintained to regulate plant physiological and developmental functions, including photoprotection, root development, seed dormancy, and pigmentation. I have identified a R2-R3 transcription factor, AtMYB2, which regulates this balance by repressing the expression of two genes, CHALCONE SYNTHASE (CHS) and FLAVONOL SYNTHASE (FLS). In myb2-ko, a knockout mutant of AtMYB2, developmental alterations, such as short roots, low production of seeds, and increased levels of pigmentation, were observed. Histochemical staining also revealed higher levels of flavonols in myb2-ko than in Col-0. The increased flavonols might disrupt the distribution of IAA and subsequently hindered root elongation. Interestingly, stimuli that induced CHS and FLS also increased the mRNA level of AtMYB2, suggesting that AtMYB2 functions to prevent overproduction of flavonols under stimuli. A gel mobility assay also showed that AtMYB2 binds to the promoter regions of CHS and FLS. My results revealed that AtMYB2 maintains homeostasis of flavonoids as well as downstream physiological and developmental function in Arabidopsis.
One major hypoxic response in plants is the switching from aerobic respiration to fermentation, which requires the induction of alcohol dehydrogenase ( ADH). Among previously isolated Arabidopsis aar mutants that are defective in ADH induction during hypoxia, I have identified aar1 as a mutation at the NPC6 locus (At3g48610), which encodes a nonspecific phospholipase C. Methyl jasmonate (MeJA) treatment resulted in an increase in the level of ADH mRNA in wild-type and aar1, albeit at a lower level. These results suggest that JA might function as a secondary messenger during hypoxia. Interestingly, hypoxia-induction of AtMYC2, a JA responsive transcription factor, is decreased in aar1. In contrast, cold induced ADH expression is not affected by the aar1 mutation. I therefore propose two signaling pathways that lead to ADH expression: a hypoxia induced pathway that requires JA, and a cold induced pathway that is independent of JA.
The main goal of my research is to elucidate the molecular mechanism by which plants respond to hypoxia (low oxygen) stress.
Dissertation Abstracts International
68-09B.
Lin, Ter-yun.
University of Iowa.
20100416135846.5
مطالعه متن کتاب [Book]
Y
