期刊
PLANT PHYSIOLOGY
卷 149, 期 1, 页码 195-204出版社
AMER SOC PLANT BIOLOGISTS
DOI: 10.1104/pp.108.128439
关键词
-
资金
- Hatch Fund [CONH00246]
- National Science Foundation [DBI-0076892]
A mutant in the maize (Zea mays) Glycolate Oxidase1 (GO1) gene was characterized to investigate the role of photorespiration in C-4 photosynthesis. An Activator-induced allele of GO1 conditioned a seedling lethal phenotype when homozygous and had 5% to 10% of wild-type GO activity. Growth of seedlings in high CO2 (1%-5%) was sufficient to rescue the mutant phenotype. Upon transfer to normal air, the go1 mutant became necrotic within 7 d and plants died within 15 d. Providing [1-C-14] glycolate to leaf tissue of go1 mutants in darkness confirmed that the substrate is inefficiently converted to (14)CO2, but both wild-type and GO-deficient mutant seedlings metabolized [1-C-14] glycine similarly to produce [C-14] serine and (CO2)-C-14 in a 1:1 ratio, suggesting that the photorespiratory pathway is otherwise normal in the mutant. The net CO2 assimilation rate in wild-type leaves was only slightly inhibited in 50% O-2 in high light but decreased rapidly and linearly with time in leaves with low GO. When go1 mutants were shifted from high CO2 to air in light, they accumulated glycolate linearly for 6 h to levels 7-fold higher than wild type and 11-fold higher after 25 h. These studies show that C-4 photosynthesis in maize is dependent on photorespiration throughout seedling development and support the view that the carbon oxidation pathway evolved to prevent accumulation of toxic glycolate.
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