| 19106015 |
Yu K, Wei J, Ma Q, Yu D, Li J: Senescence of aerial parts is impeded by exogenous gibberellic acid in herbaceous perennial Paris polyphylla. J Plant Physiol. 2009 May 15;166(8):819-30. Epub 2008 Dec 21.
The effects of gibberellin A (3) (GA (3)) on natural senescence and the relationship between gibberellins (GAs), abscisic acid (ABA), and senescence are not fully understood. For example, it is still unclear whether GA and ABA act antagonistically. There are only few reports on senescence-related changes in physiological parameters of herbaceous perennials. This study was designed to investigate the effects of exogenous GA (3) on the senescence of aerial parts in a herbaceous perennial species, Paris polyphylla, and to test the hypothesis that GA and ABA display antagonistic effects in this process. Physiological changes associated with senescence, in particular of the hormonal and oxidative metabolisms, were also investigated. GA (3) was sprayed on mature leaves at weekly intervals, which significantly impeded senescence of aerial parts and slowed the decline of pigments and total soluble protein. Treated plants suffered less oxidative stress as revealed by reduced lipid peroxidation, a lower hydrogen peroxide level and modified activities of superoxide dismutase, peroxidase, ascorbate peroxidase, and their respective isozyme profiles. In GA (3) treated plants GA (4)+GA (7) (GAs) levels increased progressively and became significantly higher than those of control plants, whereas ABA increased in controls. When plants were treated with GA-synthesis inhibitor paclobutrazol (PCB), GAs decreased, ABA increased, and senescence was promoted. Application of a mixture of GA (3) and PCB restored the accumulation of GAs, reduced ABA, and ultimately senescence was delayed. These results suggest that GA and ABA play antagonistic roles in the senescence of aerial parts in P. polyphylla, and this process is associated with oxidative stress and regulated by endogenous hormones and extrinsic factors. Possible mechanisms that control this GA (3)-mediated inhibition of senescence are discussed. |
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