Photorespiration-deficient Mutants of Arabidopsis thaliana Lacking Mitochondrial Serine Transhydroxymethylase Activity

Abstract
Three allelic mutants of Arabidopsis thaliana which lack mitochondrial serine transhydroxymethylase activity due to a recessive nuclear mutation have been characterized. The mutants were shown to be deficient both in glycine decarboxylation and in the conversion of glycine to serine. Glycine accumulated as an end product of photosynthesis in the mutants, largely at the expense of serine, starch, and sucrose formation. The mutants photorespired CO2 at low rates in the light, but this evolution of photorespiratory CO2 was abolished by provision of exogenous NH3. Exogenous NH3 was required by the mutants for continued synthesis of glycine under photorespiratory conditions. These and related results with wild-type Arabidopsis suggested that glycine decarboxylation is the sole site of photorespiratory CO2 release in wild-type plants but that depletion of the amino donors required for glyoxylate amination may lead to CO2 release from direct decarboxylation of glyoxylate. Photosynthetic CO2 fixation was inhibited in the mutants under atmospheric conditions which promote photorespiration but could be partially restored by exogenous NH3. The magnitude of the NH3 stimulation of photosynthesis indicated that the increase was due to the suppression of glyoxylate decarboxylation. The normal growth of the mutants under nonphotorespiratory atmospheric conditions indicates that mitochondrial serine transhydroxymethylase is not required in C3 plants for any function unrelated to photorespiration.