High glycolate oxidase activity is required for survival of maize in normal air

Amutant in the maize (Zea mays) Glycolate Oxidase1 (GO1) gene was characterized to investigate the role of photorespiration in C₄ 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 [1-¹⁴C]glycolate to leaf tissue of go1 mutants in darkness confirmed that the substrate is inefficiently converted to ¹⁴CO₂, but both wild-type and GO-deficient mutant seedlings metabolized [1-¹⁴C]glycine similarly to produce [¹⁴C]serine and ¹⁴CO₂ 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% O₂ in high light but decreased rapidly and linearly with time in leaves with low GO. When go1 mutants were shifted from high CO ₂ 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 C₄ 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.