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The function of ascorbate oxidase in tobacco
Cristina Pignocchi1, John M Fletcher, Joy E Wilkinson
1Crop Performance and Improvement Division, Rothamsted Research, Harpenden, Herts, AL5 2JQ, United Kingdom.
Plant Physiology
|July 15, 2003
Summary
Ascorbate oxidase (AO) enzyme activity in tobacco influences apoplastic ascorbate levels and plant growth. AO expression interacts with light, hormone, and redox signals, impacting plant development.
Area of Science:
- Plant Physiology
- Biochemistry
- Molecular Biology
Background:
- Ascorbate oxidase (AO) is an apoplastic enzyme involved in plant growth and development.
- Light and hormones significantly influence plant metabolic pathways and gene expression.
Purpose of the Study:
- To investigate the function of apoplastic ascorbate oxidase (AO) in tobacco (Nicotiana tabacum).
- To determine the impact of altered AO expression on ascorbate levels, plant growth, and responses to light and hormones.
Main Methods:
- Investigated AO mRNA abundance under different light conditions and hormonal treatments (salicylic acid, auxin).
- Generated transgenic tobacco plants with sense and antisense AO expression to manipulate apoplastic AO activity.
- Assessed whole leaf and apoplastic ascorbate (AA) content, plant height, and biomass in transformed plants.
Main Results:
- AO mRNA levels were up-regulated by light and auxin, and down-regulated by salicylic acid, correlating with growth changes.
- Altered apoplastic AO activity dramatically affected apoplastic AA levels but had minimal impact on whole leaf AA content.
- Modified AO expression altered the relationship between AO activity and plant height/biomass, and abolished light/dark regulation of native AO transcripts.
Conclusions:
- Apoplastic AO activity plays a crucial role in regulating ascorbate redox state and influences plant growth and biomass.
- AO expression integrates signals from light, hormones, and redox status in the apoplast.
- Modulating AO activity offers a potential strategy to influence plant development through redox homeostasis.