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Herbicide overexpression

Gullner, G., Komives, T., and Rennenberg, H., 2001, Enhanced tolerance of transgenic poplar plants overexpressing y-glutamylcysteine synthetase towards chloroacetanilide herbicides, / Exp. Bot. 52 971-979. [Pg.106]

GSTs also play an important role in resistance to chemical toxicity. GSTs have been implicated in resistance to the effects of a variety of chemicals including antibiotics, anticancer agents, analgesics, herbicides, insecticides, and vasodilators. Preneoplastic lesions, tumors, and cultured tumor cell lines commonly overexpress GSTs of the classes alpha, mu, and pi. This overexpression of GSTs is considered partly responsible for the resistance often associated with these cells to cancer chemotherapeutics. [Pg.234]

Interfering with protein function using specific inhibitors or antibodies. There are many protein inhibitors of metabolic enzymes that, when overexpressed, could have the potential to inhibit specific enzymatic steps (e.g., Ref. ). Nonprotein inhibitors of metabolic enzymes are also extensively used, resulting in some potent plant herbicides for which resistance can be easily manipulated, or in the formation of new compounds, when nonessential pathways are inhibited. ]... [Pg.2192]

The specificity of the whole cells and isolated photosynthetic materials was obtained by applyir the knowledge available on the relationships between herbicide binding activity and the structure of the D1 protein. For example, distinctions among classes of chemicals could be achieved through mutations in amino acid residues of D1 which can impart resistance to individual triazine herbicides. Realisation of new, sophisticated transduction systems based on printed electrodes, fluorescence and chemiluminescence as well as alternative systems such as the reconstimtion of Qp site in overexpressed DI protein utilizing chromophore quinones to enhance sensitivity and specificity for detected signals. [Pg.152]

In general, herbicide resistance can be achieved through four primary strategies detoxification of the herbicide to a non-phytotoxic metabolite expression of an herbicide insensitive target overexpression of the herbicide target and cellular sequestration of the herbicide away from the target. Of these, only the first two strategies have been successfully used to develop commercial products to date. Readers are referred to other reviews on herbicide resistance [3, 4]. [Pg.284]

The degree of resistance was the same in intact cells as in the enzyme assay. This indicates that the mutants contain a phytoene-desaturase enzyme which is modified in a way that herbicide interference is less effective. Further studies have excluded that the resistance in both mutants is caused by overexpression of the phytoene desaturase gene leading to an overproduction of phytoene desaturase. vVe observed cross resistance with some other hercicides interfering with phytoene desaturase like fluorochloridone. In contrast, our mutants were not resistant against fluridone. [Pg.284]


See other pages where Herbicide overexpression is mentioned: [Pg.215]    [Pg.100]    [Pg.196]    [Pg.115]    [Pg.365]    [Pg.759]    [Pg.61]    [Pg.135]    [Pg.77]    [Pg.127]    [Pg.128]    [Pg.128]    [Pg.152]    [Pg.524]    [Pg.462]    [Pg.311]    [Pg.686]    [Pg.1787]    [Pg.1788]    [Pg.218]    [Pg.2953]    [Pg.413]    [Pg.38]    [Pg.48]    [Pg.50]   
See also in sourсe #XX -- [ Pg.284 ]




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