Chloroplastic Aspartyl-tRNA Synthetase Is Required for Chloroplast Development, Photosynthesis and Photorespiratory Metabolism.

Abstract

Photorespiration is a complex metabolic process linked to primary plant metabolism and influenced by environmental factors, yet its regulation remains poorly understood. In this study, we identified the asprs3-1 mutant, which displays a photorespiratory phenotype with leaf chlorosis, stunted growth, and diminished photosynthesis under ambient CO₂, but normal growth under elevated CO₂ conditions. Map-based cloning and genetic complementation identified AspRS3 as the mutant gene, encoding an aspartyl-tRNA synthetase. AspRS3 is localised in both chloroplasts and mitochondria, with the chloroplast being the primary site of its physiological function. The AspRS3 mutation impacts the expression of plastid-encoded and photosynthesis-related genes, leading to decreased levels of chloroplast-encoded proteins such as ribulose-1,5-bisphosphate carboxylase/oxygenase large subunit (RBCL) and ferredoxin-dependent glutamate synthase (Fd-GOGAT). Furthermore, we observed an accumulation of photorespiratory intermediates, including glycine and glycerate, and reactive oxygen species (ROS) in asprs3-1. However, under high CO₂, the expression of these proteins, the accumulation of photorespiratory intermediates, and ROS levels in asprs3-1 did not significantly differ from those in the wild type. We propose that elevated CO₂ mitigates the asprs3-1 phenotype by inhibiting Rubisco oxygenation and photorespiratory metabolism. This study highlights the role of aminoacyl-tRNA synthetases in regulating photorespiration and provides new insights into its metabolic control.