Abstract
Main conclusion Genetic engineering of Arabidopsis thaliana reveals that mitochondrial serine hydroxymethyltransferase 1 (SHMT1) protein abundance does not limit the capacity of photorespiration, photosynthesis, or stomatal conductance. Abstract Photorespiration safeguards photosynthesis from negative metabolic feedback inhibition caused by Rubisco’s major oxygenation byproduct, 2-phosphoglycolate, and its downstream metabolites. Previous studies have shown that photosynthetic limitations can be alleviated by enhancing endogenous photorespiratory flux through position-specific enzyme overexpression. Here, we investigated whether overexpression of mitochondrial serine hydroxymethyltransferase 1 (SHMT1) influences this regulatory circuit. However, the 1.3-threefold increase in SHMT1 protein abundance did not affect the visual phenotype, growth, or photosynthetic gas-exchange parameters, including CO 2 assimilation rates and stomatal conductance, under either standard or photorespiration-promoting conditions. Metabolomic analyses further revealed wild-type-like steady-state accumulation patterns of photorespiratory and other primary metabolites in transgenic lines during both, illumination and darkness, respectively. These results indicate that SHMT1 is already expressed at sufficient levels in Arabidopsis wild type, as substantial increases in protein abundance did not enhance photorespiratory flux and growth under laboratory conditions.